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Tinospora cordifolia extract prevents cadmium-induced oxidative stress and hepatotoxicity in experimental rats.
Journal of Ayurveda and Integrative Medicine 2018 October 11
BACKGROUND: Cadmium (Cd) pollution is of serious concern due to its toxic effects in both humans and animals. The study investigates the protective effect of Tinospora cordifolia stem methanolic extract (TCME) on Cd induced hepatotoxicity.
OBJECTIVE: The aim of the study was to explore the hepatoprotective effects of T. cordifolia extract.
MATERIALS AND METHODS: Rats were administered orally with Cd (5 mg/kg) and TCME (100 mg/kg) for 28 days. At the end of the treatment period, serum and liver tissues homogenates were subjected to biochemical analysis.
RESULTS: Cd treated rats showed increased activities of the serum marker enzymes of liver damage such as AST and ALT along with increased levels of LPO and protein carbonyl content in liver tissues. Cd treatment also leads to decreased activities of endogenous antioxidants (SOD, CAT, GSH, GPx and GST), membrane ATPases (Na+ K+ ATPase, Ca2+ ATPase and Mg2+ K+ ATPase) and the tissue glycoprotein levels (hexose, fucose, hexosamine and sialic acid). Histological analysis revealed vacuolar degeneration of hepatocytes with focal necrosis upon Cd administration. TCME co-treatment restored the biochemical and histological alterations caused by Cd intoxication to near normal levels.
CONCLUSION: The results of the present investigation reveal the hepatoprotective nature of T.cordifolia against Cd induced hepatotoxicity.
OBJECTIVE: The aim of the study was to explore the hepatoprotective effects of T. cordifolia extract.
MATERIALS AND METHODS: Rats were administered orally with Cd (5 mg/kg) and TCME (100 mg/kg) for 28 days. At the end of the treatment period, serum and liver tissues homogenates were subjected to biochemical analysis.
RESULTS: Cd treated rats showed increased activities of the serum marker enzymes of liver damage such as AST and ALT along with increased levels of LPO and protein carbonyl content in liver tissues. Cd treatment also leads to decreased activities of endogenous antioxidants (SOD, CAT, GSH, GPx and GST), membrane ATPases (Na+ K+ ATPase, Ca2+ ATPase and Mg2+ K+ ATPase) and the tissue glycoprotein levels (hexose, fucose, hexosamine and sialic acid). Histological analysis revealed vacuolar degeneration of hepatocytes with focal necrosis upon Cd administration. TCME co-treatment restored the biochemical and histological alterations caused by Cd intoxication to near normal levels.
CONCLUSION: The results of the present investigation reveal the hepatoprotective nature of T.cordifolia against Cd induced hepatotoxicity.
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