Limits...
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.

Show MeSH

Related in: MedlinePlus

Effect of CCl4 with or without prior administration of natansnin on SOD levels in liver homogenate and mitochondria. Superoxide dismutase levels were estimated in homogenate, mitochondrial fragment and pure mitochondria from control, CCl4 and natansnin (10 mg/kg, 20 mg/kg body weight) treated rats. Values are given as percent control, and are mean ± S.D. of at least four animals. 0.3 mg of homogenate protein and 0.1 mg protein of sample (mitochondrial fragment and mitochondria) were used for each assay. Super oxide dismutase activity is expressed as units per mg protein. The control values of super oxide dismutase of homogenate and mitochondrial fragment and intact mitochondria were 2.88 ± 0.19, 3.08 ± 0.21 and 4.73 ± 0.25 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
getmorefigures.php?uid=PMC2967507&req=5

Figure 4: Effect of CCl4 with or without prior administration of natansnin on SOD levels in liver homogenate and mitochondria. Superoxide dismutase levels were estimated in homogenate, mitochondrial fragment and pure mitochondria from control, CCl4 and natansnin (10 mg/kg, 20 mg/kg body weight) treated rats. Values are given as percent control, and are mean ± S.D. of at least four animals. 0.3 mg of homogenate protein and 0.1 mg protein of sample (mitochondrial fragment and mitochondria) were used for each assay. Super oxide dismutase activity is expressed as units per mg protein. The control values of super oxide dismutase of homogenate and mitochondrial fragment and intact mitochondria were 2.88 ± 0.19, 3.08 ± 0.21 and 4.73 ± 0.25 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: The effect of CCl4 with and without the prior administration of natansnin on levels of catalase activity was shown in Figure 3. The activity of catalase decreased in both homogenate and mitochondria by 56 and 53% respectively in CCL4 treated rats. (Control = 733.9 ± 38.9 nmol/min/mg protein in homogenate and 1453 ± 64.6 nmol/min/mg protein in mitochondria. CCl4 = 323.7 ± 24.7 nmol/min/mg protein in homogenate and 685.05 ± 35.7 nmol/min/mg protein in mitochondria). But there is a significant increase in the catalase activity in both homogenate and mitochondria in rats administered with natansnin and CCl4 when compared to rats administered with only CCl4. Prior administration of natansnin at 10 mg/kg body wt protected them up to 35% (582.8 ± 30.1 nmol/min/mg protein) and 32% (1150.9 ± 54.8 nmol/min/mg protein) and at 20 mg/kg body wt the protection was slightly better 38.64% (593.6 ± 34.3 nmol/min/mg protein) and 36.06% (1190.8 ± 56.2 nmol/min/mg protein) in homogenate and mitochondria respectively. There was no significant effect on catalase levels in rats administered with natansnin alone. The effect of CCl4 in the presence and absence of natansnin on the activity of superoxide dismutase is shown in Figure 4. The activity of superoxide dismutase decreased in homogenate, mitochondrial fragment and mitochondria by 47 (1.51 ± 0.11 units/mg protein), 52 (1.48 ± 0.10 units/mg protein) and 57 (2.10 ± 0.25 units/mg protein) % respectively due to the effect of CCl4, when compared to normal rats (received only mineral oil). There was a considerable increase in the activity of SOD in all the fragments in rats fed with both concentrations of natansnin and CCl4, when compared to rats administered with only CCl4. The treatment of natansnin at lower dose (10 mg/kg body wt) protected the animals by 25% (2.22 ± 0.13 units/mg protein), 32% (2.47 ± 0.16 units/mg protein) and 32% (3.60 ± 0.19 units/mg protein) and at higher dose (20 mg/kg body wt) by 29% (2.30 ± 0.14 units/mg protein), 37% (2.47 ± 0.15 units/mg protein) and 36% (3.79 ± 0.23 units/mg protein) respectively. The activity of superoxide dismutase increased in natansnin treated rats, when compared to rats that were challenged with CCl4. Administration of natansnin alone did not show any change on SOD levels 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 SOD levels in liver homogenate and mitochondria. Superoxide dismutase levels were estimated in homogenate, mitochondrial fragment and pure mitochondria from control, CCl4 and natansnin (10 mg/kg, 20 mg/kg body weight) treated rats. Values are given as percent control, and are mean ± S.D. of at least four animals. 0.3 mg of homogenate protein and 0.1 mg protein of sample (mitochondrial fragment and mitochondria) were used for each assay. Super oxide dismutase activity is expressed as units per mg protein. The control values of super oxide dismutase of homogenate and mitochondrial fragment and intact mitochondria were 2.88 ± 0.19, 3.08 ± 0.21 and 4.73 ± 0.25 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 4: Effect of CCl4 with or without prior administration of natansnin on SOD levels in liver homogenate and mitochondria. Superoxide dismutase levels were estimated in homogenate, mitochondrial fragment and pure mitochondria from control, CCl4 and natansnin (10 mg/kg, 20 mg/kg body weight) treated rats. Values are given as percent control, and are mean ± S.D. of at least four animals. 0.3 mg of homogenate protein and 0.1 mg protein of sample (mitochondrial fragment and mitochondria) were used for each assay. Super oxide dismutase activity is expressed as units per mg protein. The control values of super oxide dismutase of homogenate and mitochondrial fragment and intact mitochondria were 2.88 ± 0.19, 3.08 ± 0.21 and 4.73 ± 0.25 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: The effect of CCl4 with and without the prior administration of natansnin on levels of catalase activity was shown in Figure 3. The activity of catalase decreased in both homogenate and mitochondria by 56 and 53% respectively in CCL4 treated rats. (Control = 733.9 ± 38.9 nmol/min/mg protein in homogenate and 1453 ± 64.6 nmol/min/mg protein in mitochondria. CCl4 = 323.7 ± 24.7 nmol/min/mg protein in homogenate and 685.05 ± 35.7 nmol/min/mg protein in mitochondria). But there is a significant increase in the catalase activity in both homogenate and mitochondria in rats administered with natansnin and CCl4 when compared to rats administered with only CCl4. Prior administration of natansnin at 10 mg/kg body wt protected them up to 35% (582.8 ± 30.1 nmol/min/mg protein) and 32% (1150.9 ± 54.8 nmol/min/mg protein) and at 20 mg/kg body wt the protection was slightly better 38.64% (593.6 ± 34.3 nmol/min/mg protein) and 36.06% (1190.8 ± 56.2 nmol/min/mg protein) in homogenate and mitochondria respectively. There was no significant effect on catalase levels in rats administered with natansnin alone. The effect of CCl4 in the presence and absence of natansnin on the activity of superoxide dismutase is shown in Figure 4. The activity of superoxide dismutase decreased in homogenate, mitochondrial fragment and mitochondria by 47 (1.51 ± 0.11 units/mg protein), 52 (1.48 ± 0.10 units/mg protein) and 57 (2.10 ± 0.25 units/mg protein) % respectively due to the effect of CCl4, when compared to normal rats (received only mineral oil). There was a considerable increase in the activity of SOD in all the fragments in rats fed with both concentrations of natansnin and CCl4, when compared to rats administered with only CCl4. The treatment of natansnin at lower dose (10 mg/kg body wt) protected the animals by 25% (2.22 ± 0.13 units/mg protein), 32% (2.47 ± 0.16 units/mg protein) and 32% (3.60 ± 0.19 units/mg protein) and at higher dose (20 mg/kg body wt) by 29% (2.30 ± 0.14 units/mg protein), 37% (2.47 ± 0.15 units/mg protein) and 36% (3.79 ± 0.23 units/mg protein) respectively. The activity of superoxide dismutase increased in natansnin treated rats, when compared to rats that were challenged with CCl4. Administration of natansnin alone did not show any change on SOD levels 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