Protective role of puerarin on lead-induced alterations of the hepatic glutathione antioxidant system and hyperlipidemia in rats |
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Authors: | Chan-Min Liu Jie-Qiong Ma Yun-Zhi Sun |
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Affiliation: | aSchool of Life Science, Xuzhou Normal University, No. 101, Shanghai Road, Tangshan New Area, Xuzhou City 221116, Jiangsu Province, PR China;bSchool of Chemical Engineering, China University of Mining and Technology, Xuzhou City 221008, Jiangsu Province, PR China |
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Abstract: | Puerarin (PU), a natural flavonoid, has been reported to have many benefits and medicinal properties. The aim of the present study was to investigate the effects of puerarin on hepatic oxidative stress and hyperlipidemia in rats exposed to lead. Our data showed that puerarin significantly prevented lead-induced hepatotoxicity, indicated by both diagnostic indicators of liver damage (serum aminotransferase levels) and histopathological analysis. Moreover, lead-induced profound elevation of ROS production and oxidative stress, as evidenced by increasing of lipid peroxidation level, reducing of GPx, GST, GR and GCL activities and depleting of intracellular reduced GSH level in liver, were suppressed by treatment with puerarin. Furthermore, the increase of serum cholesterol, triglycerides and LDL induced by lead was effectively suppressed by puerarin. The HDL level in the lead treatment rats was also increased by puerarin. Western blot analysis showed that puerarin remarkably inhibited hyperlipidemia by regulating the expression of cholesterol 7a-hydroxylase (CYP7A1), 3-hydroxy-3-methylglutaryl-CoA reductase (HMGR) and low-density lipoprotein receptor (LDL-R) in liver of lead treated rats. Altogether, these results suggest that puerarin could protect the lead-induced liver injury and hyperlipidemia by reducing ROS production, renewing the activities of antioxidant enzymes and influencing expression of hepatic lipid biosynthesis and metabolism genes. |
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Keywords: | Abbreviations: ALT, alanine aminotransferase AST, aspartate aminotransferase CAT, catalase CYP7A1, cholesterol 7a-hydroxylase GCL, Glutamate&ndash cysteine ligase GPx, glutathione peroxidase GR, glutathione reductase GSH, reduced glutathione GSSG, oxidized glutathione GST, glutathione S-transferase HDL, high-density lipoproteins HMGR, 3-hydroxy-3-methylglutaryl-CoA reductase LDL, low-density lipoproteins LDL-R, low-density lipoprotein receptor Pb, lead PU, puerarin ROS, reactive oxygen species SOD, superoxide dismutase TBARS, thiobarbituric acid reactive substances |
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