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Puerarin exerts the protective effect against chemical induced dysmetabolism in rats
- Li, Rong, Song, Jianhua, Wu, Wei, Wu, Xinmou, Su, Min
- Gene 2016 v.595 no.2 pp. 168-174
- Toll-like receptor 4, actin, alanine transaminase, apoptosis, aspartate transaminase, blood sampling, blood serum, carbon tetrachloride, caspase-3, collagen, gene expression regulation, glucose tolerance, glucose tolerance tests, high density lipoprotein cholesterol, histology, insulin, intraperitoneal injection, islets of Langerhans, liver, liver cirrhosis, liver function, low density lipoprotein cholesterol, messenger RNA, protective effect, rats, smooth muscle, tumor necrosis factor-alpha
- In this study, we aim to explore the potential benefits of puerarin on metabolic function of liver fibrosis (LF) rat induced by carbon tetrachloride (CCl4), and to investigate with the underlying molecular mechanism targeted on liver and pancreas tissues. In methodology, The LF rats were prepared through intragastrically giving CCl4 twice each week (2ml/kg, v/w) for 8weeks, and dosed puerarin (20, 40mg/kg) were given three times each week via intraperitoneal injection. After being conducted with oral glucose tolerance test (OGTT), the blood samples of rat were harvested for biochemical tests, as well as the liver and pancreas were isolated for histological examination and biochemical assays. The findings showed that puerarin-administered rats resulted in reduced glucose tolerance, blood insulin level, sero-enzymes of alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and increased plasma level of high-density lipoprotein cholesterol (HDL-C) and reduced low-density lipoprotein cholesterol (LDL-C) content in serum. Further, the intrahepatic collagen deposits were lessened and positive cell of alpha smooth muscle actin (α-SMA) was lessened in puerarin treatment, while the pro-apoptotic cell numbers of Caspase 3, Bax in pancreatic islets were reduced dose-dependently. Moreover, the mRNA expressions of toll-like receptor 4 (TLR4) and tumor necrosis factor (TNF-α) in liver and pancreas were downregulated. In addition, TNF-α protein in the CCl4-lesioned liver and pancreas was reduced. Our findings demonstrate that puerarin contributes to attenuating the metabolic dysfunctions of CCl4-damaged liver and pancreas, in which the possible mechanisms may be linked to inhibition of inflammatory stress and normalization of metabolic homoeostasis in the liver and pancreas.