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Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl4 induced oxidative stress and cellular degeneration in rat liver.

Srilaxmi P, Sareddy GR, Kavi Kishor PB, Setty OH, Babu PP - BMC Pharmacol. (2010)

Bottom Line: Natansnin treatment significantly decreased the levels of CCl4 induced apoptotic proteins and inflammatory mediators.Further natansinin treatment significantly inhibited the CCl4 induced apoptosis which was evident form the reduced TUNEL positive cells.This protective effect of natansnin can be correlated to its direct antioxidant effect.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Genetics, Osmania University, Hyderabad, India.

ABSTRACT

Background: Carbon tetra chloride (CCl4), an industrial solvent, is a hepatotoxic agent and it is the well established animal model for free radical-induced liver injury. The present investigation was carried out to establish the protective effect of natansnin, a novel dibenzoyl glycoside from Salvinia natans against CCl4 induced oxidative stress and cellular degeneration in rat liver.

Results: CCl4 significantly increased the levels of lipid peroxides, oxidized glutathione and decreased the levels of reduced glutathione, SOD and CAT. CCl4 induce marked histopathological changes and increase in the levels of apoptotic proteins. CCl4 treatment significantly increased the levels of apoptotic proteins such as caspases-3, PARP, Bax, Bid and cytochrome C and also increased the levels of inflammatory mediators iNos and Cox-2. Natansnin treatment significantly decreased the levels of CCl4 induced apoptotic proteins and inflammatory mediators. Further natansinin treatment significantly inhibited the CCl4 induced apoptosis which was evident form the reduced TUNEL positive cells.

Conclusions: In conclusion, our study demonstrated the protective effect of natansnin against CCl4 induced oxidative stress and cellular degeneration in rat liver tissue. This protective effect of natansnin can be correlated to its direct antioxidant effect.

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Effect of CCl4 with or without prior administration of natansnin on lipid peroxide level in liver homogenate and mitochondria. Homogenate and mitochondrial fractions were isolated from control, CCl4 and natansnin (10 mg/kg, 20 mg/kg body weight) treated rats and lipid peroxides were estimated using thiobarbituric acid reaction method. Values are given as percent control, and are mean ± S.D. of at least four animals. Lipid peroxide levels were expressed as nmol MDA formed per 100 mg protein. The control values in homogenate and mitochondria are 135.2 ± 8.6, 121.4 ± 6.6 respectively. a = Statistical significant at P < 0.05 as compare to control, b = Statistical significant at P < 0.05 as compare to CCl4, c = Statistical significant at P < 0.05 as compare to CCl4+ natansnin (10 mg).
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Figure 1: Effect of CCl4 with or without prior administration of natansnin on lipid peroxide level in liver homogenate and mitochondria. Homogenate and mitochondrial fractions were isolated from control, CCl4 and natansnin (10 mg/kg, 20 mg/kg body weight) treated rats and lipid peroxides were estimated using thiobarbituric acid reaction method. Values are given as percent control, and are mean ± S.D. of at least four animals. Lipid peroxide levels were expressed as nmol MDA formed per 100 mg protein. The control values in homogenate and mitochondria are 135.2 ± 8.6, 121.4 ± 6.6 respectively. a = Statistical significant at P < 0.05 as compare to control, b = Statistical significant at P < 0.05 as compare to CCl4, c = Statistical significant at P < 0.05 as compare to CCl4+ natansnin (10 mg).

Mentions: Effect of the administration of CCl4 with and without the prior administration of natansnin on lipid peroxide level is shown in Figure 1. In homogenate and mitochondria, the lipid peroxide levels significantly increased (80 and 118% respectively) due to the administration of CCl4 compared to controls. (Control = 135.2 ± 8.6 nmol/100 mg protein in homogenate and 121.4 ± 6.6 nmol/100 mg protein in mitochondria) (CCl4 = 244.3 ± 10.1 nmol/100 mg protein in homogenate and 265.3 ± 11.2 nmol/100 mg protein). There was a significant decrease in the level of lipid peroxides in both homogenate and mitochondria, in natansnin and CCl4 treated rats. Prior administration of 10 mg/kg body wt of natansnin offered a protection rate of 61 and 86% in homogenate (161.5 ± 7.8 nmol/100 mg protein) and mitochondria (161.4 ± 7.5 nml/100 mg protein). With an increase of natansnin to 20 mg/kg body wt, protection rate increased only marginally 63 and 88% in homogenate (159.4 ± 7.5 nmol/100 mg protein) and (158.6 ± 7.2 nmol/100 mg protein) mitochondria respectively. Administration of natansnin alone did not show any change on formation of lipid peroxides when compared to control animals.


Protective efficacy of natansnin, a dibenzoyl glycoside from Salvinia natans against CCl4 induced oxidative stress and cellular degeneration in rat liver.

Srilaxmi P, Sareddy GR, Kavi Kishor PB, Setty OH, Babu PP - BMC Pharmacol. (2010)

Effect of CCl4 with or without prior administration of natansnin on lipid peroxide level in liver homogenate and mitochondria. Homogenate and mitochondrial fractions were isolated from control, CCl4 and natansnin (10 mg/kg, 20 mg/kg body weight) treated rats and lipid peroxides were estimated using thiobarbituric acid reaction method. Values are given as percent control, and are mean ± S.D. of at least four animals. Lipid peroxide levels were expressed as nmol MDA formed per 100 mg protein. The control values in homogenate and mitochondria are 135.2 ± 8.6, 121.4 ± 6.6 respectively. a = Statistical significant at P < 0.05 as compare to control, b = Statistical significant at P < 0.05 as compare to CCl4, c = Statistical significant at P < 0.05 as compare to CCl4+ natansnin (10 mg).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2967507&req=5

Figure 1: Effect of CCl4 with or without prior administration of natansnin on lipid peroxide level in liver homogenate and mitochondria. Homogenate and mitochondrial fractions were isolated from control, CCl4 and natansnin (10 mg/kg, 20 mg/kg body weight) treated rats and lipid peroxides were estimated using thiobarbituric acid reaction method. Values are given as percent control, and are mean ± S.D. of at least four animals. Lipid peroxide levels were expressed as nmol MDA formed per 100 mg protein. The control values in homogenate and mitochondria are 135.2 ± 8.6, 121.4 ± 6.6 respectively. a = Statistical significant at P < 0.05 as compare to control, b = Statistical significant at P < 0.05 as compare to CCl4, c = Statistical significant at P < 0.05 as compare to CCl4+ natansnin (10 mg).
Mentions: Effect of the administration of CCl4 with and without the prior administration of natansnin on lipid peroxide level is shown in Figure 1. In homogenate and mitochondria, the lipid peroxide levels significantly increased (80 and 118% respectively) due to the administration of CCl4 compared to controls. (Control = 135.2 ± 8.6 nmol/100 mg protein in homogenate and 121.4 ± 6.6 nmol/100 mg protein in mitochondria) (CCl4 = 244.3 ± 10.1 nmol/100 mg protein in homogenate and 265.3 ± 11.2 nmol/100 mg protein). There was a significant decrease in the level of lipid peroxides in both homogenate and mitochondria, in natansnin and CCl4 treated rats. Prior administration of 10 mg/kg body wt of natansnin offered a protection rate of 61 and 86% in homogenate (161.5 ± 7.8 nmol/100 mg protein) and mitochondria (161.4 ± 7.5 nml/100 mg protein). With an increase of natansnin to 20 mg/kg body wt, protection rate increased only marginally 63 and 88% in homogenate (159.4 ± 7.5 nmol/100 mg protein) and (158.6 ± 7.2 nmol/100 mg protein) mitochondria respectively. Administration of natansnin alone did not show any change on formation of lipid peroxides when compared to control animals.

Bottom Line: Natansnin treatment significantly decreased the levels of CCl4 induced apoptotic proteins and inflammatory mediators.Further natansinin treatment significantly inhibited the CCl4 induced apoptosis which was evident form the reduced TUNEL positive cells.This protective effect of natansnin can be correlated to its direct antioxidant effect.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Genetics, Osmania University, Hyderabad, India.

ABSTRACT

Background: Carbon tetra chloride (CCl4), an industrial solvent, is a hepatotoxic agent and it is the well established animal model for free radical-induced liver injury. The present investigation was carried out to establish the protective effect of natansnin, a novel dibenzoyl glycoside from Salvinia natans against CCl4 induced oxidative stress and cellular degeneration in rat liver.

Results: CCl4 significantly increased the levels of lipid peroxides, oxidized glutathione and decreased the levels of reduced glutathione, SOD and CAT. CCl4 induce marked histopathological changes and increase in the levels of apoptotic proteins. CCl4 treatment significantly increased the levels of apoptotic proteins such as caspases-3, PARP, Bax, Bid and cytochrome C and also increased the levels of inflammatory mediators iNos and Cox-2. Natansnin treatment significantly decreased the levels of CCl4 induced apoptotic proteins and inflammatory mediators. Further natansinin treatment significantly inhibited the CCl4 induced apoptosis which was evident form the reduced TUNEL positive cells.

Conclusions: In conclusion, our study demonstrated the protective effect of natansnin against CCl4 induced oxidative stress and cellular degeneration in rat liver tissue. This protective effect of natansnin can be correlated to its direct antioxidant effect.

Show MeSH
Related in: MedlinePlus