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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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Related in: MedlinePlus

Effect of CCl4 with or without prior administration of natansnin on histological characteristics. Haematoxylin and Eosin staining was performed in liver sections of control (a, b), CCl4 (c, d) and natansnin (10 mg/kg (e), 20 mg/kg (f) body weight) treated rats. An Arrow symbol represents fatty vacuoles and lattice nature of the hepatocytes.
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Figure 5: Effect of CCl4 with or without prior administration of natansnin on histological characteristics. Haematoxylin and Eosin staining was performed in liver sections of control (a, b), CCl4 (c, d) and natansnin (10 mg/kg (e), 20 mg/kg (f) body weight) treated rats. An Arrow symbol represents fatty vacuoles and lattice nature of the hepatocytes.

Mentions: Paraffin wax sectioning and Haematoxylin-Eosin staining were performed for histopathological studies of rats. Haematoxylin-Eosin staining of control liver had normal cell morphology and is shown in Figure 5a and 5b. The histoarchitecture of hepatic cells of CCl4 challenged rats is shown in Figure 5c and 5d. The hepatic cells of natansnin and CCl4 treated rats are shown in Figure 5e and 5f. When compared to the histoarchitecture of the hepatocytes of control animals, hepatocytes of CCl4 challenged rats revealed extensive damage, characterized by the disruption of lattice nature of the hepatocyte, damaged cell membrane, degenerated nuclei and increased fatty vacuolation. In Group 4 and 5 rats (exposed to natansnin + CCl4), only minimal disruption of the hepatic cellular structure and less vacuolation were noticed. Prior administration of natansnin decreased the cellular degeneration, compared to CCl4 treated hepatocytes. Hepatocyte apoptosis in fixed liver specimens were analyzed by terminal dUTP nick- end labeling (TUNEL) assay. TUNEL sections of control, CCl4 treated and natansnin and CCl4 treated rats are shown in Figures 6a, b, c, d, e and 6f respectively. The number of TUNEL positive hepatocytes is more in CCl4 treated rats, when compared to controls indicating an increase in apoptotic degeneration of hepatocytes. Apoptosis in CCl4 treated liver was identified by the BrdU- FITC (green fluorescence at DNA nicks). BrdU-FITC is incorporated into the DNA breaks that were increased during free radical generation and apoptotic cell death pathway. Elevated levels of FITC fluorescent hepatocytes indicate the increased apoptosis of CCl4 treated liver hepatocytes over the control. The number of apoptotic cells was significantly reduced in both the concentrations of natansnin and CCl4 treated rats (6e and 6f) as evident from the decrease in TUNEL positive hepatocytes. Prior administration of natansnin decreased the number of apoptotic cells, when compared to CCl4 challenged hepatocytes (6c and 6d).


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 histological characteristics. Haematoxylin and Eosin staining was performed in liver sections of control (a, b), CCl4 (c, d) and natansnin (10 mg/kg (e), 20 mg/kg (f) body weight) treated rats. An Arrow symbol represents fatty vacuoles and lattice nature of the hepatocytes.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

Figure 5: Effect of CCl4 with or without prior administration of natansnin on histological characteristics. Haematoxylin and Eosin staining was performed in liver sections of control (a, b), CCl4 (c, d) and natansnin (10 mg/kg (e), 20 mg/kg (f) body weight) treated rats. An Arrow symbol represents fatty vacuoles and lattice nature of the hepatocytes.
Mentions: Paraffin wax sectioning and Haematoxylin-Eosin staining were performed for histopathological studies of rats. Haematoxylin-Eosin staining of control liver had normal cell morphology and is shown in Figure 5a and 5b. The histoarchitecture of hepatic cells of CCl4 challenged rats is shown in Figure 5c and 5d. The hepatic cells of natansnin and CCl4 treated rats are shown in Figure 5e and 5f. When compared to the histoarchitecture of the hepatocytes of control animals, hepatocytes of CCl4 challenged rats revealed extensive damage, characterized by the disruption of lattice nature of the hepatocyte, damaged cell membrane, degenerated nuclei and increased fatty vacuolation. In Group 4 and 5 rats (exposed to natansnin + CCl4), only minimal disruption of the hepatic cellular structure and less vacuolation were noticed. Prior administration of natansnin decreased the cellular degeneration, compared to CCl4 treated hepatocytes. Hepatocyte apoptosis in fixed liver specimens were analyzed by terminal dUTP nick- end labeling (TUNEL) assay. TUNEL sections of control, CCl4 treated and natansnin and CCl4 treated rats are shown in Figures 6a, b, c, d, e and 6f respectively. The number of TUNEL positive hepatocytes is more in CCl4 treated rats, when compared to controls indicating an increase in apoptotic degeneration of hepatocytes. Apoptosis in CCl4 treated liver was identified by the BrdU- FITC (green fluorescence at DNA nicks). BrdU-FITC is incorporated into the DNA breaks that were increased during free radical generation and apoptotic cell death pathway. Elevated levels of FITC fluorescent hepatocytes indicate the increased apoptosis of CCl4 treated liver hepatocytes over the control. The number of apoptotic cells was significantly reduced in both the concentrations of natansnin and CCl4 treated rats (6e and 6f) as evident from the decrease in TUNEL positive hepatocytes. Prior administration of natansnin decreased the number of apoptotic cells, when compared to CCl4 challenged hepatocytes (6c and 6d).

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