Salutary Effect of Ferulic Acid Against D-Galactosamine Challenged Liver Damage
In the present study, we evaluated the effect of Ferulic Acid (FA) supplementation (20 mg kg super(-1) body weight) on GalN provoked hepatotoxicity in male Wistar rats. Hepatotoxicity was induced by a single intraperitoneal injection of GalN (500 mg kg super(-1) body weight) and manifested by an inc...
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Veröffentlicht in: | Journal of biological sciences (Faisalabad, Pakistan) Pakistan), 2008-11, Vol.8 (8), p.1271-1279 |
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Sprache: | eng |
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Zusammenfassung: | In the present study, we evaluated the effect of Ferulic Acid (FA) supplementation (20 mg kg super(-1) body weight) on GalN provoked hepatotoxicity in male Wistar rats. Hepatotoxicity was induced by a single intraperitoneal injection of GalN (500 mg kg super(-1) body weight) and manifested by an increase in the levels hepatospecific marker enzymes like Aspartate Transaminase (AST), Alanine Transaminase (ALT), Alkaline Phosphatase (ALP) and Lactate Dehydrogenase (LDH). In contrast, pretreatment with FA significantly ameliorated all these alterations. GalN intoxicated rats visualize a remarkable oxidative stress, as evidenced by a significant elevation in Lipid Peroxidation (LPO) with a concomitant decrease in the glutathione (GSH) activity. These changes were coupled with a marked decline in the activities of enzymic antioxidants [superoxide dismutase (SOD), catalase (CAT), Glutathione Peroxidase (GPx) and Glutathione Reductase (GR)] in the liver tissue of GalN administered rats. FA pretreated rats exhibit a significant inhibition of LPO and augmentation of endogenous antioxidants. Further, there was an increase in the levels of cholesterol, triglycerides and free fatty acids followed by a decrease in the levels of phospholipids in serum and liver. Pretreatment with FA reversed these alterations to near normal. Results of this study revealed that FA could afford a significant protection in the alleviation of GalN induced hepatocellular injury. |
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ISSN: | 1727-3048 |
DOI: | 10.3923/jbs.2008.1271.1279 |