Acetic Acid Induce Vascular Permeability Biology Essay

Body weight of the animate beings before and after expiration was noted and no any important alteration observed. Further tegument and pelt, eyes and mucose membranes and besides respiratory, circulatory, autonomic and cardinal nervous system and somatomotor activity and behaviour form were besides unchanged. Additionally, there was no any mark of shudders, paroxysm, salivation, diarrhea ; lethargy, sleep and coma were noted. The oncoming of toxicity and marks of toxicity besides noted but found negative.

The acute unwritten toxicity survey was done harmonizing to the OECD guidelines 423 ( Acute Toxic Method ) . A get downing dosage used was 2000 mg/kg, p. o. of TPF and TPR was administered to 3 male rats, observed for three yearss. There was no considerable alteration in organic structure weight before and after intervention of the experiment and no marks of toxicity were observed. When the experiments were repeated once more with the same dose degree, 2000 mg/kg, p. o. of methanolic infusions of flower and root for 3 yearss more and observed for 14 yearss, no alteration were observed from the first set of experiment. LD50 cut off mg/kg organic structure weight was observed as X-unclassified.

The TPF and TPR did non bring forth deadliness up to the dose degree of 2000 mg/kg.

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5.2.2 Anti-inflammatory activity

5.2.2.1. Acetic acid bring on vascular permeableness ( acute survey )

Methanolic infusions of the works were reduced the extent of peritoneal redness induced by injection of acetic acid. The optical density was well ( P & A ; lt ; 0.01 ) reduced in all doses of TPF and TPR. Standard drug intervention Indomethacin exhibited strongest activity with 65.31 % suppression in dye escape as compared to command. ( Table 6.34 ) TPF and TPR at the dosage of 400 mg/kg were exhibits 61.58 % and 52.49 % suppression severally.

Similarly, FEA and REA were besides reduced the sum of dye escape and, the decrease in vascular permeableness by FEA ( 31.94 % ) and REA ( 22.65 % ) was found to be 31.94 % ( P & A ; lt ; 0.05 ) and 22.65 % correspondingly. The consequence demonstrated by ethyl ethanoate infusions was lesser as compared with the consequence produced by the methanolic infusions. ( Table 6.35 )

Table 6.34: Consequence of TPF and TPR on acetic acid induced vascular permeableness in mice.

Groups

Dose ( mg/kg )

Absorbance #

% suppression

Control

CMC

1.848 ± 0.12

0

Indo

5

0.641 ± 0.10**

65.31

TPF

100

1.560 ± 0.15

15.58

200

1.141 ± 0.04*

38.26

400

0.710 ± 0.11**

61.58

TPR

100

1.564 ± 0.09

15.37

200

1.397 ± 0.10

24.40

400

0.878 ± 0.80**

52.49

# Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Table 6.35: Consequence of FEA and REA on acetic acid induced vascular permeableness in mice.

Groups

Dose ( mg/kg )

Absorbance #

% Inhibition

Control

CMC

1.85 ± 0.12

0

Indo

5

0.64 ± 0.10**

65.36

FEA

100

1.82 ± 0.12

1.42

200

1.43 ± 0.21

22.71

400

1.26 ± 0.15*

31.94

REA

100

1.84 ± 0.12

0.58

200

1.55 ± 0.20

16.27

400

1.43 ± 0.23

22.65

# Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

5.2.2.2. Cotton pellet induced granuloma in rats ( chronic survey )

Table 6.36 shows chronic anti-inflammatory effects of the TPF and TPR at the doses of 100, 200 and 400 mg/kg. Changes in the cotton pellets weights ( wet weight-dry weight ) of the trial substances were compared with the controls. TPF and TPR showed important ( P & A ; lt ; 0.01 ) , dose dependent chronic anti-inflammatory consequence. TPF and TPR ( 400 mg/kg ) showed 37.06 % and 31.25 % suppression severally ; whereas Indo treated group exhibited 46.52 % . Their effects are in comparable magnitude with the standard anti-inflammatory drug.

However, FEA and REA at the dosage of 400 mg/kg were showed 28.03 % and 20.81 % suppression in granuloma formation severally and found to be statistically important ( P & A ; lt ; 0.01 ) as compared with control group. At low dosage ( 100 mg/kg ) both FEA and REA does non suppress the granuloma formation. Standard compound Indocin was showed 42.20 % suppression. The suppression observed in in-between group of FEA and REA besides lesser but statistically important ( P & A ; lt ; 0.05, P & A ; lt ; 0.01 ) ( Table 6.37 )

Table 6.36: Consequence of TPF and TPR on % suppression on cotton pellet induced chronic redness in rats

Groups

Dose ( mg/kg )

Wet weight ( g ) #

Dry weight ( g ) #

Difference ( g )

% Inhibition

Control

CMC

154.62± 2.04

56.87± 3.70

97.75

0.00

Indo

10

73.98±2.03**

21.7±1.03**

52.28

46.52

TPF

100

138.57±2.40*

41.05±1.61**

97.52

0.24

200

108.87±4.37*

33.47±1.18**

75.4

22.86

400

84.12±2.25**

22.6± 1.24**

61.52

37.06

TPR

100

142.18±1.87*

44.62±1.87**

97.56

0.19

200

120.33±1.50*

38.83±1.82**

81.5

16.62

400

96.23±1.56**

29.03±2.96**

72.57

31.25

# Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Table 6.37: Consequence of FEA and REA on % suppression on cotton pellet induced chronic redness in rats

Groups

Dose ( mg/kg )

Wet weight ( g ) #

Dry weight ( g ) #

Difference ( g )

% suppression

Control

CMC

150.62± 1.36

55.87± 3.17

94.75

0

Indo

10

79.45± 1.37**

24.68±1.64**

54.77

42.20

FEA

100

138.83±1.90**

44.71±1.64**

94.12

0.66

200

112.55±2.99**

37.67±1.81**

74.88

20.97

400

96.0± 3.21**

27.81±1.46**

68.19

28.03

REA

100

141.35± 1.05*

47± 2.87*

94.35

0.42

200

122.38±2.36**

40.67±1.81**

81.71

13.76

400

107.88±3.09**

32.85±0.99**

75.03

20.81

# Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

5.2.3 Analgesic activity

5.2.3.1. Formalin induce nociception in mice ( Chemical initiation )

Table 6.38 depicts the consequence of TPF and TPR on formol induce nociceptive response in mice. As shown, all the three doses of the TPF and TPR were significantly ( P & A ; lt ; 0.01 ) impaired the clip spent on defeat of injected paw, both in the early ( 0- 5 min ) and late stages ( 15- 30 min ) of nociception. However, the consequence in the early stage appears to be instead higher than in the late stage.

While, FEA ( 400 gm/kg ) REA ( 400 mg/kg ) treated group shows statistically important ( P & A ; lt ; 0.01 ) decrease in nociceptive response in both early and late stages. REA treated groups produced slightly lesser extent of consequence in both stages as compared to FEA intervention. ( Table 6.39 )

Table 6.38: Consequence of TPF and TPR on nociceptive response on formol induced nociception in mice

Groups

Dose

( mg/kg )

Nociceptive response ( sec ) #

% suppression

Early Phase

Late stage

Early stage

Late stage

Control

CMC

58.1± 1.09

39.28± 1.04

Penta

2

13.52 ± 1.36**

7.98± 1.06**

76.73

79.68

TPF

100

44.77± 1.70*

33.38± 1.70

22.94

15.02

200

35.1± 1.48*

20.57± 1.19*

39.59

47.63

400

18.3± 1.47**

13.7± 1.41**

68.50

65.12

TPR

100

44.63± 1.13*

36.37± 2.27

23.18

7.41

200

36.43± 1.51*

34.7± 1.16*

37.29

11.66

400

24.07± 1.03**

16.34± 1.08**

58.57

58.40

# Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Table 6.39: Consequence of FEA and REA on nociceptive response on formol induced nociception in mice

Groups

Dose

Nociceptive response ( s ) #

% suppression

Early Phase

Late stage

Early stage

Late stage

Control

CMC

69.23± 2.07

47.62± 1.16

Penta

2

13.23± 1.18*

9.43± 1.10**

80.89

80.20

FEA

100

50.52± 1.23*

36.52± 1.52*

27.03

23.31

200

42.48± 0.91*

26.02± 2.03**

38.64

45.36

400

34.32± 1.28**

22.37± 1.03**

50.43

53.02

REA

100

57.45± 1.65*

45.63± 1.55

17.02

4.18

200

40.35± 0.68*

43.43± 1.89

41.72

8.80

400

34.85± 1.28*

30.32± 1.76**

49.66

36.33

# Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

5.2.3.2. Acetic acid induce wrestling in mice ( Peripheral analgesia )

Among the infusion treated groups the higher dosage of TPF ( 400 mg/kg ) was showed better ( 65.31 % ) and statistically important ( P & A ; lt ; 0.01 ) suppress the figure of writhings induced by acetic acid. Indo treated group shows grater suppression ( 73.18 % ) in Hagiographas, whereas, TPR treated animate beings were besides exhibit statistically important ( P & A ; lt ; 0.01 ) consequence with 59.48 % suppression. ( Table 6.40 ) Hence, the protective consequence shown by TPF and TPR is dose dependent.

Similarly, high dosage ( 400 mg/kg ) of FEA ( 48.34 % ) and REA ( 36.66 % ) shows better and statistically important suppression of figure of writhings. ( Table 6.41 ) Standard ( Indo, 5 mg/kg ) treated group demonstrate highest no. of decrease in wrestling ( 16.83± 0.86 ) as compared to command ( CMC suspension ) group ( 50± 1.13 ) and with 66.34 % suppression. Nevertheless, FEA and REA at medium dosage ( 200 gm/kg ) degree besides produce statistically important suppression ( P & A ; lt ; 0.01 and P & A ; lt ; 0.05 ) .

Table 6.40: Consequence of TPF and TPR on writhings induced by acetic acid in mice

Groups

Dose ( mg/kg )

No. of wrestling #

% Inhibition

Control

CMC

57.16 ± 1.50

Indo

5

15.33±1.16**

73.18

TPF

100

38±1.54**

33.53

200

32.5±0.51**

43.15

400

19.83±0.43**

65.31

TPR

100

41.83±0.43**

26.83

200

35.5±1.28**

37.9

400

23.16±1.03**

59.48

# Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Table 6.41: Consequence of FEA and REA on writhings induced by acetic acid in mice

Groups

Dose ( mg/kg )

No. of wrestling #

% Inhibition

Control

CMC

50 ± 1.13

Indo

5

16.83± 0.86**

66.34

FEA

100

43.5± 1.21*

13

200

35.16± 1.06**

29.68

400

25.83± 1.40**

48.34

REA

100

47.16± 1.47

5.68

200

39.5± 0.51*

21

400

30.67± 1.74**

36.66

# Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

5.2.3.3 Hot home base method in mice ( Thermal initiation )

TPF at the dose 400 mg/kg showed a important analgetic consequence ( P & A ; lt ; 0.01 ) against thermally induced hurting at 30, 60, 90 and 120 min of the survey period ( Table 6.42 ) , with more than 50 % protection was achieved at 60 min. TPR at the dose 400 mg/kg significantly increased the hot-plate latency clip in mice get downing from 30 min ( P & A ; lt ; 0.05 ) , at 120 min it showed the maximal protection ( ~112 % ) which is reasonably similar to TPF ( 400 mg/kg ) . By contrast, Pentazocine was shown to supply protection against thermally induced stimulations throughout the observation period ( P & A ; lt ; 0.01 at 30, 60, 90 and 120 min ) , with maximal protection ( ~157 % ) conferred after 120 min.

FEA and REA at the dose 400 mg/kg were showed a important analgetic consequence ( P & A ; lt ; 0.01 ) against thermally induced hurting at 60, 90 and 120 min of the survey period ( Table 10 ) , with 90.06 % and 80 % protection was achieved at 60 min severally. REA at the dose 400 mg/kg significantly increased the hot-plate latency clip in mice get downing from 60 min ( P & A ; lt ; 0.01 ) , at 90 min it showed the maximal protection ( ~98 % ) which is to some extent lesser than FEA ( 400 mg/kg ) .

Ethyl ethanoate infusions were shown to hold lesser extent of % protection against nociception in thermic initiation than methanolic infusions. Additionally, ethyl ethanoate infusions were produced higher grade of activity at 90 min ; after, the analgetic action gets decreased bit by bit. By contrast, methanolic infusion may demo similar grade of activity like standard drug Pentazocine.

Table 6.42: Consequence of TPF and TPR on latency clip and % protection against thermic initiation on hot home base method in mice

Groups

Dose

( mg/kg )

Latency time/ reaction clip # in sec ( % PATI )

Pre drug

Rotational latency

30 min

60 min

90 min

120 min

Control

CMC

4.34± 0.17

4.41± 0.18

4.8± 0.46

4.93± 0.44

6.14± 0.47

Penta

2

5.07± 0.21

6.60± 0.51**

( 30.18 )

10.25± 0.64**

( 102.17 )

13.18± 0.51**

( 159.96 )

13.06± 0.72**

( 157.59 )

TPF

100

4.78± 0.24

5.03± 0.15

( 5.23 )

7.55± 0.41**

( 57.95 )

7.12± 0.42*

( 48.95 )

8.39± 0.44*

( 62.30 )

200

5.12± 0.39

5.29± 0.35

( 3.32 )

6.73± 0.34*

( 31.45 )

8.31± 0.57**

( 62.30 )

9.92± 0.40**

( 93.75 )

400

5.37± 0.26

7.33± 0.49**

( 36.50 )

8.63± 0.52**

( 60.71 )

11.03± 0.75**

( 105.40 )

11.41± 0.41**

( 112.48 )

TPR

100

4.59± 0.31

4.78± 0.22

( 4.14 )

6.82± 0.41*

( 48.58 )

7.82± 0.54**

( 70.37 )

8.33± 0.35*

( 81.48 )

200

5.37± 0.26

4.77± 0.23

( -11.17 )

7.04± 0.29*

( 31.10 )

8.06± 0.53**

( 68.72 )

8.8± 0.38**

( 63.87 )

400

4.49± 0.25

5.9± 0.51*

( 31.40 )

7.81± 0.73**

( 73.94 )

9.1± 0.47**

( 102.67 )

9.54± 0.53**

( 112.47 )

Valuess in parenthesis indicate the % protection against thermic initiation ( PATI ) . # Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Table 6.43: Consequence of FEA and REA on latency clip and % protection against thermic initiation on hot home base method in mice

Groups

Dose ( mg/kg )

Latency time/ reaction clip # in sec ( % PATI )

pre drug latency

30 min

60 min

90 min

120 min

Control

CMC

4.97± 0.38

5.07± 0.49

5± 0.38

5.55± 0.35

4.97± 0.18

Penta

2

5.18± 0.40

7.81±0.40** ( 50.77 )

10.89±0.45** ( 110.23 )

12.38±0.95** ( 139.0 )

12.97±0.20** ( 150.39 )

FEA

100

4.83± 0.35

6.01± 0.52 ( 24.43 )

6.96± 0.30* ( 44.10 )

8.53± 0.52* ( 76.60 )

8.05± 0.26* ( 66.67 )

200

5.28± 0.29

5.19± 0.49 ( -1.70 )

7.12± 0.31* ( 34.85 )

9.88± 0.42* ( 87.12 )

8.53± 0.31* ( 61.55 )

400

5.03± 0.45

6.44± 0.51 ( 28.03 )

9.56±0.41** ( 90.06 )

10.38± 0.72** ( 106.36 )

9.59±0.53** ( 90.66 )

REA

100

5.77± 0.43

5.25± 0.50 ( -9.01 )

7.33± 0.55* ( 27.04 )

8.6± 0.52* ( 49.05 )

7.63± 0.19* ( 32.24 )

200

5.68± 0.33

6.15± 0.59 ( 8.27 )

7.43± 0.32* ( 30.81 )

9.98± 0.71* ( 75.70 )

8.78± 0.28* ( 54.58 )

400

4.85± 0.53

6.37± 0.34 ( 31.34 )

8.73±0.41** ( 80.0 )

9.59± 0.44** ( 97.73 )

8.44±0.29** ( 74.02 )

Valuess in parenthesis indicate the % protection against thermic initiation ( PATI ) . # Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

5.2.4 Anti-arthritis activity

5.2.4.1. Freund ‘s adjuvant induced arthritis in rat

Consequence of on primary lesions

The observation made on different yearss of intervention period in freund ‘s complete adjuvant induced arthritis showed that there was a less increased in paw swelling in DF and infusions treated animate beings as compared to command group. The appraisal made on the 21st twenty-four hours showed that, intervention with all infusions every bit good as DF significantly ( P & A ; lt ; 0.01 ) cut down the injected paw swelling ( primary lesions ) as compared with control group. The TPF, TPR, FEA and REA at the doses of 400 mg/kg, p.o. showed per centum suppression in average paw volume by 70.37 % , 62.96 % , 58.02 % and 49.38 % severally. While, DF intervention group showed 80.25 % per centum suppression in average paw volume on twenty-four hours 21. ( Table 6.44 )

Additionally, photographic images of injected paw of animate beings were besides assisting to uncover the protective effects of infusion and DF intervention. ( Fig. 6.66 )

Consequence of on organic structure weight

Changes in organic structure weight have besides been used to measure the class of the disease and the response to therapy of anti-inflammatory drugs as the incidence and badness of arthritis increased, the alterations in the organic structure weight of the rat besides occurred during the class of experimental period. The organic structure weight decrease was less for groups which received DF ( 3.8 g ) and TPF ( 4.6 g ) ( Table 6.45 ) when compared to command group ( 16.5 g ) . TPR, FEA and REA at dosage of 400 mg/kg, p.o. showed statistically important ( P & A ; lt ; 0. 01 ) decrease in weight as compared with control group.

Table 6.44: Consequence of TPF, TPR, FEA and REA on Injected Paw Volume ( Primary Lesions ) in CFA induced arthritis in rat.

Groups

Dose ( mg/kg )

Average addition in paw volume # ( milliliter )

Day 5

Day 10

Day 15

Day 20

Control

CMC

0.43 ± 0.03

0.66 ± 0.01

0.82 ± 0.01

0.81 ± 0.01

DF

5

0.27 ± 0.01** ( 37.21 )

0.31± 0.02** ( 53.03 )

0.31± 0.02** ( 62.20 )

0.16± 0.02** ( 80.25 )

TPF

400

0.29 ± 0.01** ( 32.56 )

0.33± 0.02** ( 50.0 )

0.34± 0.01** ( 58.54 )

0.24± 0.02** ( 70.37 )

TPR

0.31 ± 0.01** ( 27.91 )

0.38± 0.01** ( 42.42 )

0.43± 0.01** ( 47.56 )

0.30± 0.02** ( 62.96 )

FEA

0.37 ± 0.03 ( 13.95 )

0.48± 0.03** ( 27.27 )

0.58± 0.08** ( 29.27 )

0.53± 0.07** ( 34.57 )

REA

0.40 ± 0.05 ( 6.98 )

0.51± 0.04** ( 22.73 )

0.59± 0.08** ( 28.03 )

0.57± 0.02** ( 29.63 )

Valuess in parenthesis indicate the % suppression. # Valuess are expressed as average ± SEM. n=6 ** P & A ; lt ; 0.01 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

* P & A ; lt ; 0.05, ** P & A ; lt ; 0.01 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Fig 6.66: Showing consequence of TPF, TPR, FEA and REA on % rise in ankle diameter of injected paw in FCA induced arthritis in rats.

control2

2 mg2

a. Control

b. DF ( 5 mg/ kilogram )

10 milligram

5 mg2

c. REA ( 400 mg/kg )

d. FEA ( 400 mg/kg )

2 mg1

std2

e. TPR ( 400 mg/kg )

f. TPF ( 400 mg/kg )

Fig 6.67: Showing the exposure of injected paw in FCA induced arthritis in rats taken at 21st twenty-four hours of the survey.

Table 6.45: Consequence of TPF, TPR, FEA and REA on organic structure weight in CFA induced arthritis in rat.

Group

Dose ( mg/kg )

Mean organic structure weight # ( gram )

Decrease in organic structure weight ( gram )

0 twenty-four hours

21 twenty-four hours

Control

CMC

178.5 ± 1.088

162.0 ± 0.96

16.5

DF

5

188.5 ± 2.094

184.7 ± 1.78**

3.8

TPF

400

198.3 ± 4.645

193.7 ± 3.99**

4.6

TPR

201 ± 4.351

195.5 ± 2.43**

5.5

FEA

197.8 ± 4.498

188.3 ± 1.62**

9.5

REA

202 ± 3.512

190.2 ± 2.09**

11.8

# Valuess are expressed as average ± SEM. n=6 * P & A ; lt ; 0.05, ** P & A ; lt ; 0.01 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Consequence on hiting systems

Arthritis mark is increased from day-7 to day-21, the maximal mark was peaked at 21st twenty-four hours. ( Table 6.46 ) All infusions were showed dose dependent decrease in arthritis mark as compared to vehicle treated group. Among the infusions TPF showed maximal consequence at dosage of 400 mg/kg, p.o. and comparable to the group treated with standard drug DF.

Flexure hurting trial mark was employed to measure consequence of extract intervention on suppression of creaky hurting. This trial mark additions as disease advancement takes topographic point. All infusions and DF decreases flexure hurting trial mark on day-7 and day- 21 in a dose dependent mode. ( Table 6.46 )

Consequences of mobility mark are shown in Table 6.46. All infusions at the dosage of 400 mg/kg p.o. showed mensurable decrease in mobility mark ( 3-1 ) on 21st twenty-four hours. Decrease in mobility mark on 14th twenty-four hours is slightly less but in a dose dependent mode.

In instance of stance hiting system the maximal mark referred to the normal status of animate beings while decrease in mark indicates badness of disease patterned advance. Consequence of TPF, TPR, FEA and REA on stance mark was observed and it found to be dose dependent and comparable with the consequence of DF. ( Table 6.46 )

Table 6.46: Consequence of TPF, TPR, FEA and REA on assorted pain trial tonss in FCA induced arthritis in rat.

Groups

Dose ( mg/kg )

Arthritis mark

Flexure hurting

trial Mark

Mobility mark

Stance mark

Control

CMC

4 ( 4,3 )

3 ( 3,3 )

3 ( 3,3 )

1 ( 1,1 )

DF

5

2 ( 4,2 ) **

1 ( 2,1 ) **

1.5 ( 2,1 ) **

2 ( 2,1 ) **

REA

400

3.5 ( 4,3 )

2.5 ( 3,2 ) *

2.5 ( 3,2 )

3 ( 3,1 )

FEA

4 ( 4,3 )

2.5 ( 3,2 ) *

3 ( 3,2 )

2.5 ( 3,1.5 )

TPR

3.5 ( 4,3 )

2 ( 3,2 ) *

2 ( 3,2 ) **

2 ( 3,2 ) **

TPF

3 ( 4,2 )

2.5 ( 3,1 ) *

2 ( 3,1 ) **

2 ( 3,1 ) **

Valuess are expressed as median ( maximal, lower limit ) . n=6 * P & A ; lt ; 0.05, ** P & A ; lt ; 0.01 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Consequence on hematologic parametric quantities

A ) Entire leucocyte ( WBC ) count

In arthritis status there is a mild to chair rise in the WBC count due to let go of of IL-1 & A ; szlig ; inflammatory response. Entire leukocyte count was found to be decreased in infusion and DF treated groups as compared to command group. The WBC count in TPF treated group at dosage of 400 mg/kg, p.o. has count of 9.59 – 103 /mm3, while DF treated group showed WBC count of 9.53 -103/mm3 ( Fig 6.67 )

B ) Haemoglobin

The consequences indicated that hemoglobin count was normalized in TPF and DF treated group as compared to command group ( Fig 6.68 ) . This indicates protective consequence of TPF against anaemia that occurs due to creaky status. However, ethyl ethanoate infusion ( 400 mg/kg, p.o. ) treated groups did non showed important degree of hemoglobin as compared to the control group.

* P & A ; lt ; 0.05, ** P & A ; lt ; 0.01 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Fig 6.67: Showing consequence of TPF, TPR, FEA and REA on WBC count in FCA induced arthritis in rats.

** P & A ; lt ; 0.01 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Fig 6.68: Showing consequence of TPF, TPR, FEA and REA on hemoglobin count in FCA induced arthritis in rats.

C ) Erythrocyte deposit rate ( ESR )

The consequence indicated that, ESR was likewise lowered in TPF ( 3.54 mm/ hour ) and DF ( 3.42 mm/ hour ) treated group as compared to command group ( Fig 6.69 ) . Besides, TPR at 400 mg/kg p.o. treated group showed significantly ( P & A ; lt ; 0.01 ) lowered values for ESR as compared to the control group.

** P & A ; lt ; 0.01 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Fig 6.69: Showing consequence of TPF, TPR, FEA and REA on Erythrocyte ( RBC ) deposit rate ( ESR ) in FCA induced arthritis in rats.

D ) Concentration of C- reactive protein ( CRP )

The rate of synthesis and secernment of CRP is additions within hours of an acute hurt or the oncoming of redness. So, if CRP concentration is greater than 0.6 mg/dL a seeable agglutination is observed in the presence of CRP latex reagent. The degrees of CRP in serum were measured by semi-quantitative method. Methanolic infusions ( 400 mg/kg, p.o. ) and DF significantly ( P & A ; lt ; 0.01 ) lowered the degree of CRP as compared to command. ( Fig 6.70 ) . CRP degree in TPF ( 400 mg/kg, p.o. ) treated group ( 2 mg/dL ) was lower than that of the DF treated group ( 1.8 mg/dL ) .

* P & A ; lt ; 0.05, ** P & A ; lt ; 0.01 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Fig 6.70: Showing consequence of TPF, TPR, FEA and REA on concentration of CRP in FCA induced arthritis in rats.

Tocopherol ) Concentration of arthritic factor ( RF )

Any serum sample incorporating 10 IU/mL or more of arthritic factor will demo a clear agglutination. The degrees of RF in serum were measured semi-quantitatively. In this survey, serum sample of control showed 73.33 IU/mL of RF. TPF, TPR, FEA and REA 400 mg/kg, p.o. showed significantly lowered concentration of RF at concentration of 30, 33.33, 46.67 and 53.33 IU/mL severally. The concentrations of RF in TPF ( 400 mg/kg, p.o. ) treated group was reasonably similar to that of the positive control group treated with DF ( Fig 6.71 ) .

* P & A ; lt ; 0.05, ** P & A ; lt ; 0.01 when compared with control ( ANOVA followed by Dunnett ‘s t-test ) .

Fig 6.71: Showing consequence of TPF, TPR, FEA and REA on concentration of RF in FCA induced arthritis in rats.

5.2.5 Anti- hyperlipidemic activity

5.2.5.1 in- vivo survey

5.2.5.1.1. High fat diet ( HFD ) induce lipemia ( hyper-cholesterolemia ) in rats ( Chronic survey )

High fat diet disposal in animate beings was showed increased serum degrees of cholesterin ( 236.8 mg/dl ) , triglyceride ( 229 mg/dl ) and lipoproteins [ LDL-c ( 164.3 mg/dl ) , VLDL-c ( 45.80 mg/dl ) ] nevertheless, the HDL-c degree get decreased to 26.63 mg/dl. Administration of TPF ( 400 mg/kg/p.o. ) to HFD rats consequences in important ( P & A ; lt ; 0.01 ) decreased in the degree of serum cholesterin ( 160.3 mg/dl ) ( Fig 6.72 ) , triglyceride ( 138.7 mg/dl ) ( Fig 6.73 ) , LDL-c ( 91.34 mg/dl ) ( Fig 6.74 ) and VLDL-c ( 27.73 mg/dl ) ( Fig 6.75 ) , with important ( P & A ; lt ; 0.01 ) addition in HDL-c degree by 41.95 mg/dl ( Fig 6.76 )

All infusion treated groups were showed the important ( P & A ; lt ; 0.05, P & A ; lt ; 0.01 ) decrease in serum cholesterin degree. TPF and TPR at higher dosage ( 400 mg/kg ) were found to be more important ( P & A ; lt ; 0.01 ) among the trial groups as they showed reduced serum degree of triglyceride, LDL-c, VLDL-c and increased serum degree of HDL-c. Standard drug Simvastatin ( Sim, 4 mg/kg ) exhibited statistically important ( P & A ; lt ; 0.01 ) and highest grade of protective consequence throughout the survey.

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HFD ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.72: Consequence of TPF and TPR on serum cholesterin degree in HFD induced lipemia in rats.

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HFD ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.73: Showing consequence of TPF and TPR on serum triglyceride degree in HFD induced lipemia in rats.

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HFD ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.74: Showing consequence of TPF and TPR on serum LDL-c degree in HFD induced lipemia in rats.

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HFD ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.75: Showing consequence of TPF and TPR on serum VLDL-c degree in HFD induced lipemia in rats.

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HFD ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.76: Showing consequence of TPF and TPR on serum HDL-c degree in HFD induced lipemia in rats.

While, the animate beings treated with Simvastatin ( Sim, 4 mg/kg ) and TPF ( 400 mg/kg ) were showed important ( P & A ; lt ; 0.01 ) lessening in organic structure weight as compared to HFD group when measured on twenty-four hours 20 and twenty-four hours 30. Finally, the mean organic structure weight of animate beings of HFD, Sim and TPF ( 400 mg/kg ) treated group was found to be 267.3 g, 207.0 g and 221 g severally ( Table 6.47 ) . At the concluding twenty-four hours, HFD showed 50.23 % rise in initial organic structure weight, as compared to this the TPR and TPF ( 400 mg/kg ) were demonstrated 32.98 % and 25.17 % rise, and for Sim ( 4 mg/kg ) it was found to be 17.13 % .

Table 6.47: Consequence of TPF and TPR on organic structure weight in HFD induced lipemia in rats.

Groups

Dose ( mg/kg )

Mean organic structure weight # ( g )

Initial

Day 10

Day 20

Day 30

Control

CMC

174.8±7.43

183.0±10.2

193.8±5.17

195.2±3.41

HFD

179.0±5.03

214.2±4.93 ( 19.54 )

231.2±7.28 ( 30.62 )

267.3±8.10 ( 50. 23 )

HFD + Sim

4

177.3±3.19

187.2±3.70 ( 5.56 )

197.0±6.80** ( 11.14 )

207.0±5.97** ( 17.13 )

HFD + TPR

100

171.3±6.67

196.5±6.00 ( 14.92 )

215.0 ±6.43 ( 25.51 )

243.0±9.37* ( 43.04 )

HFD + TPR

200

174.0±4.67

195.7±3.57 ( 12.59 )

212.2±3.71 ( 19.79 )

240.5±3.79* ( 38.69 )

HFD + TPR

400

176.7±4.30

195.7±5.53 ( 10.73 )

202.8±5.52** ( 15.39 )

234.0±2.41** ( 32.98 )

HFD + TPF

100

170.3±5.57

197.2±4.92 ( 16.01 )

213.3±5.91 ( 26.62 )

240.2±9.04* ( 42.0 )

HFD + TPF

200

177.8±4.07

197.2±3.80 ( 11.01 )

207.7±3.71* ( 19.45 )

237.7±3.82** ( 33.91 )

HFD + TPF

400

177.5±3.45

185.0±5.47 ( 4.46 )

203.2±4.76** ( 14.58 )

221.0±3.89** ( 25.17 )

Valuess in parenthesis indicates % rise in initial organic structure weight, # Valuess are expressed as average ± SEM. n = 6. *P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HFD group ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.77 showed the consequence of TPF and TPR on atherogenic index. However, merely Simvastatin ( Sim, 4 mg/kg ) and the TPF ( 400 mg/kg ) were showed important ( P & A ; lt ; 0.01 ) atherogenic index as compared to HDF treated group.

Fig 6.77: Showing consequence of TPF and TPR on atherogemnic index in HFD induced lipemia in rats.

5.2.5.1.2. Triton WR 1339-induced lipemia in rats ( acute survey )

Triton WR-1339 has causes a pronounced addition in cholesterin and triglyceride serum concentrations after intraperitoneal injection ( 200 mg/kg ) as compared to normal group. Coincident disposal of TPF and TPR at the dosage of ( 100 and 200 mg/kg ) does non demo important decrease in entire cholesterin, triglyceride, VLDL, LDL when compared with Triton treated group. Whereas standard drug Gemfibrozil ( 250 mg/kg ) and TPF ( 400 mg/kg ) shows important ( P & A ; lt ; 0.01 ) decrease in lipid profile as compared to triton treated group.

Fig 6.78 depicts the consequence of methanolic infusions on cholesterin degree. TPF ( 400 mg/kg ) showed important decrease in serum cholesterin degree in 24 and 48 hour after Triton injection. Gemfibrozil ( Gem, 250 mg/kg ) displayed reasonably greater consequence with serum cholesterin degree 127.1 mg/dl ( 24 hour, P & A ; lt ; 0.01 ) and 86.45 mg/dl ( 48 hour, P & A ; lt ; 0.01 )

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HCG ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.78: Showing consequence of TPF and TPR on serum cholesterin degree in Triton induced lipemia in rats.

Consequence of TPF and TPR on serum triglyceride degree was summarized in Fig 6.79 Methanolic infusions did non showed important ( P & A ; gt ; 0.05 ) decrease in serum triglyceride degree, excepting TPF ( 400 mg/kg ) which was showed statistically important ( P & A ; lt ; 0.05 ) decrease after 24 hour of the Triton injection. On the other manus, Gemfibrozil ( Gem, 250 mg/kg ) showed important decrease in triglyceride degree at 24 hour ( P & A ; lt ; 0.01 ) and 48 hour ( P & A ; lt ; 0.05 ) as compared to hyperlipidemic control group treated group.

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HCG ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.79: Showing consequence of TPF and TPR on serum triglyceride degree in Triton induced lipemia in rats.

The standard drug Gemfibrozil ( 250 mg/kg ) significantly ( P & A ; lt ; 0.01 ) increase the serum degree of HDL-c at 24 and 48 hour as compared to hyperlipidemic control group. TPF and TPR besides showed addition in serum HDL-c degree ; nevertheless, it was non found to be important statistically. For, hyperlipidemic control group the HDL-c degree was 37.45 mg/dl ( 24 hour ) and 38.20 mg/dl ( 48 hour ) and for TPF ( 400 mg/kg ) it was 37.36 mg/dl ( 24 hour ) and 40.84 mg/dl ( 48 hour ) . Hence, the methanolic infusions did non exhibit any considerable increase in the degree of serum HDL-c. TPR ( 400 mg/kg ) ( Fig 6.80 )

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HCG ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.80: Showing consequence of TPF and TPR on serum HDL-c degree in Triton induced lipemia in rats.

Similar consequence was observed with TPF and TPR on serum LDL-c degree. Merely TPF at higher dosage ( 400 mg/kg ) showed statistically important ( P & A ; lt ; 0.01 ) decrease in LDL-c degree after 48 hour. While, gemfibrozil demonstrated the important ( P & A ; lt ; 0.01 ) consequence at 24 hour ( 14.22 mg/dl ) and 48 hour ( 22.19 mg/dl ) as compared to hyperlipidemic control group which showed LDL-c degree 45.86 mg/dl at 24 hour and 50.79 mg/dl at 48 hour severally. Although staying trial infusions were showed decrease in serum LDL-c degree but it was non- important ( P & A ; gt ; 0.05 ) . ( Fig 6.81 )

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HCG ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.81: Showing consequence of TPF and TPR on serum LDL-c degree in Triton induced lipemia in rats.

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with HCG ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.82: Showing consequence of TPF and TPR on serum VLDL-c degree in Triton induced lipemia in rats.

5.2.5.1.3. Hypolipidemic activity in rats

Methanolic infusions were tested for hypolipidemic activity in normal rats kept on normal diet. Simvastatin ( 4 mg/kg ) was used as mention criterion for the survey which shows important lessening in Serum cholesterin ( P & A ; lt ; 0.05 ) , triglyceride ( P & A ; lt ; 0.01 ) and VLDL-c degree ( P & A ; lt ; 0.05 ) nevertheless HDL-c degree was significantly ( P & A ; lt ; 0.01 ) increased as compared to command group.

TPF and TPR did non bring forth any important alterations in serum cholesterin degree in normal rats ( Fig 6.83 ) . But at the higher dosage ( 400 mg/kg ) TPF and TPR reasonably reduced the cholesterin degree but it was n’t found to be important. Cholesterol degree for control group was about 91.92 mg/dl and for Simvastatin it was 78.84 gm/dl.

*P & A ; lt ; 0.05, when compared with control ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.83: Showing consequence of TPF and TPR on serum Cholesterol degree in hypolipidemic in rats.

Serum triglyceride degree was significantly reduced by TPF ( 400 mg/kg ) ( P & A ; lt ; 0.05 ) and Simvastatin ( Sim, 4 mg/kg ) ( P & A ; lt ; 0.01 ) as compared to command. Staying doses of infusions were showed any mensurable alteration in triglyceride degree. For Simvastatin, TPF ( 400 mg/kg ) and control ; triglyceride degree was 106.2 gm/dl, 110.2 mg/dl and 128.6 mg/dl severally.

*P & A ; lt ; 0.05, **P & A ; lt ; 0.001, when compared with control ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.84: Showing consequence of TPF and TPR on serum triglyceride degree in hypolipidemic in rats.

Concurrently, serum HDL-c degree did non found to be statistically important in TPF and TPR treated group. Practically, TPF ( 400 mg/kg ) was proved to increase the degree ( 46.29 gm/dl ) of HDL-c in normal rats, but it was non statistically important ( P & A ; gt ; 0.05 ) . Simvastatin ( Sim, 4 mg/kg ) treated group showed statistically important ( P & A ; lt ; 0.01 ) rise in protective HDL-c degree about to 55 mg/dl as compared to command group ( 41.19 mg/dl )

**P & A ; lt ; 0.001, when compared with control ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.85: Showing consequence of TPF and TPR on serum HDL-c degree in hypolipidemic in rats.

Similarly, all the infusion and Simvastatin treated groups did non exhibits the statistically important decrease in serum LDL-c degree. Although, there was found to be somewhat decrease in Sim ( 4 mg/kg ) ( 24.80 gm/dl ) and TPF ( 400 mg/kg ) ( 27.69 gm/dl ) group but non important ( P & A ; gt ; 0.05 ) as compared to command group ( 31.54 gm/dl ) .

Fig 6.86: Showing consequence of TPF and TPR on serum LDL-c degree in hypolipidemic in rats.

Again, in instance of serum VLDL-c degree, merely Simvastatin ( 4 mg/kg ) treated group showed important ( P & A ; lt ; 0.05 ) decrease. Staying extract treated groups did non change the VLDL-c degree in the serum to a important ( P & A ; gt ; 0.05 ) degree. TPF at higher the dosage of 400 mg/kg was showed little decrease ( 27.69 gm/dl ) in VLDL-c degree as compared to command group degree ( 31.54 gm/dl ) .

*P & A ; lt ; 0.05, when compared with control ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.87: Showing consequence of TPF and TPR on serum triglyceride degree in hypolipidemic in rats.

5.2.5.1.4. HMG-CoA Reductase enzyme activity

The ratio of HMG-CoA / Mevalonate ratio was significantly ( P & A ; lt ; 0.01 ) increased by the standard drug Simvastatin ( Sim, 4 mg/kg ) ( 3.29 ) whereas, TPF and TPR at a dosage of 400 mg/kg were besides exhibited important addition in the ratio as compared to command group. The in-between dosage ( 200 mg/kg ) of both the infusions did non showed statistically important consequence as compared to command group. TPF 400 mg/kg showed higher consequence ( 2.71 ) , followed by Simvastatin ; among the trial infusions. ( Fig 6.88 )

**P & A ; lt ; 0.001, when compared with control ( ANOVA followed by Dunnett ‘s t-test )

Fig 6.88: Showing consequence of TPF and TPR on HMG- CoA/ mevalonate ratio in rats.

5.2.5.2 in- vitro survey

5.2.5.2.1. Platelet anti-aggregation activity

The per centum suppression of thrombocyte collection was significantly increased with the intervention of high concentration ( 1000 ?g/ml ) of TPF ( 41.40 ) and TPR ( 33.68 ) . Whereas, intervention with standard drug, Heparin ( Hep 20 ?g/ml ) was showed highest per centum ( 79.57 ) of thrombocyte suppression. The lower concentrations of TPF and TPR were besides demonstrated anti-aggregation consequence to a certain extent. ( Table 6.48 )

Table 6.48: Consequence of TPF and TPR on thrombocyte collection induced by ADP

Groups

Concentration ( ?g/ml )

Absorbance #

% Inhibition

Adenosine diphosphate

10

2.23± 0.01

Hep

20

0.56± 0.17**

79.57

TPR

250

1.97± 0.01

16.65

500

1.82± 0.06**

23.35

1000

1.58± 0.04**

33.68

TPF

250

1.84± 0.09**

22.17

500

1.72± 0.13**

27.44

1000

1.41± 0.10**

41.40

# Valuess are expressed as average ± SEM. n = 6. * P & A ; lt ; 0.05, ** P & A ; lt ; 0.001 when compared with control ( ANOVA followed by Dunnett ‘s t-test )

5.2.5.2.2. Anti-inflammatory activity

The repressive consequence of different concentrations of TPF and TPR on protein denaturation was found to be concentration dependant are shown in Table 11. TPF and TPR at different dosage degrees ( 50 – 250 ?g/ml ) showed considerable ability to suppress denaturation of egg albumen.

Table 6.49: Consequence ( % suppression ) of TPF and TPR on protein denaturation

Drug concentration

( µg/ml )

Inhibition of protein denaturation ( % )

TPF

TPR

50

34.67 ± 0.79

24.78 ± 0.82

100

39.54 ± 0.84

30.72 ± 0.27

150

46.34 ± 0.89

39.91 ± 0.42

200

67.83 ± 0.45

52.23 ± 0.91

250

72.76 ± 0.39

64.71 ± 0.82

# Valuess are expressed as average ± SEM. n = 3.

5.2.6 Antioxidant activity

5.2.6.1 DPPH extremist scavenging activity

The consequences of the DPPH extremist scavenging activity of Ascorbic acid and all samples were shown in Fig 6.89. All the samples were produced concentration dependent decrease in optical density and rise in per centum suppression. The scavenging ability of the TPF ( IC50 44.62 ) was found to be greater among the all tested samples ; nevertheless ascorbic acid was showed DPPH extremist scavenging efficaciousness with IC50 37.79 ( Table 6.50 ) . Ethyl ethanoate infusions besides exhibits similar antiradical consequence as that of AA.

Fig 6.89: Showing consequence of TPF, TPR, FEA and REA on the DPPH extremist scavenging activity

5.2.7.2 Nitric oxide scavenging activity

TPF showed considerable scavenging of azotic oxide group as compared to standard drug. The % scavenging and IC50 valleies for ascorbic acid and TPF were 41.32 and 43.02 severally ( Table 6.50 ) . However, all the samples were exhibited concentration dependent rise in per centum suppression. The optical density of the samples was reduced as addition in concentration ( Fig 6.90 ) . The Higher concentration of each sample was showed per centum suppression about & amp ; gt ; 50 % .

Fig 6.90: Showing consequence of TPF, TPR, FEA and REA on the Nitric oxide radical scavenging activity

5.2.7.3 Anti-Lipid Peroxidation ( ALP ) By Using Liver Homogenate

Again, higher concentration of TPF shows grater anti- lipid peroxidation activity, as indicated by their % suppression values ( Table 6.50 ) ; but less every bit compared to ascorbic acid which shows about 73.80 % suppression. The degree of lipid peroxidation was suppressed concentration dependently by all the tried infusions. FEA ( 65.21 % ) and REA ( 63.94 % ) showed less suppression as compared to ascorbic acid. As concentration of sample addition the optical density of reaction mixture was decreased accordingly. ( Fig 6.91 )

Fig 6.91: Showing consequence of TPF, TPR, FEA and REA on the lipid peroxidation in rat liver homogenate

Table 6.49: Percentage suppression by AA, TPF, TPR, FEA and REA in different in-vitro antioxidant theoretical accounts

Sr. no

Conc. ( µg/mL )

DPPH Scavenging activity

Nitric Oxide Scavenging activity

Lipid Peroxidation suppression

Aa

20

27.94

36.05

24.94

40

45.16

50.89

38.23

60

63.84

58.21

51.01

80

74.02

69.73

55.57

100

85.67

82.81

73.80

TPF

20

38.09

49.97

45.71

40

43.67

54.57

51.24

60

48.81

60.48

56.58

80

63.63

65.04

62.61

100

72.92

70.77

69.20

TPR

20

39.22

37.67

38.67

40

43.41

42.72

45.13

60

47.38

52.14

49.94

80

62.30

56.66

55.27

100

70.30

63.29

60.25

FEA

20

43.79

43.95

39.57

40

48.58

48.50

45.03

60

52.52

55.91

49.89

80

55.57

61.66

57.61

100

59.49

65.20

63.94

REA

20

30.98

42.30

33.57

40

37.89

46.34

37.07

60

42.29

50.98

45.12

80

44.78

57.04

51.36

100

49.93

64.23

57.61

5.2.7.4 Reducing Power Assay

Consequently, cut downing power of all samples was found to be concentration dependent. The sample with higher optical density has greater cut downing capableness. Among the infusion the TPF showed higher cut downing power ( 0.6794±0.004 ) , and it was relatively higher than standard drug ascorbic acid ( 0.5493±0.001 ) . ( Fig 6.92 )

Fig 6.92: Showing consequence of TPF, TPR, FEA and REA on the Reducing power capacity