丹参素对四氯化碳致大鼠肝纤维化的保护作用

W. Qu , H. Huang , K. Li , C. Qin
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引用次数: 19

摘要

肝纤维化(HF)的罪魁祸首与胶原蛋白的阈上沉积有关。因此,通过改善新陈代谢减少胶原蛋白有助于心衰管理。本研究旨在探讨丹参素(DSS)对四氯化碳(CCl4)诱导的HF大鼠的肝保护作用。结果表明,大鼠给药后肝体指标明显降低,血清谷丙转氨酶(ALT)和天冬氨酸转氨酶(AST)水平明显降低。同时,DSS给药组肝组织超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性升高,丙二醛(MDA)含量降低。此外,促纤维化标志物羟脯氨酸(Hyp)、III型前胶原(PCIII)和透明质酸(HA)含量降低。组织病理学检查证实,DSS对ccl4损伤大鼠的肝毒性有所减轻。此外,肝内α-平滑肌肌动蛋白(α-SMA)、磷酸化JAK2 (p-JAK2)和磷酸化STAT3 (p-STAT3)的蛋白表达均有效下调。综上所述,本研究表明DSS对ccl4诱导的肝组织细胞毒性具有保护作用,其机制可能与抑制脂质过氧化、胶原积累、增强抗氧化防御能力以及调节肝内JAK/STAT通路维持胶原稳态有关。
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Danshensu-mediated protective effect against hepatic fibrosis induced by carbon tetrachloride in rats

The culprit of hepatic fibrosis (HF) is linked to suprathreshold deposition of collagen. Thus, collagen reduction by improved metabolism contributes to HF management. In this study, we aimed to investigate the hepatoprotective effects of Danshensu (DSS) against carbon tetrachloride (CCl4)-induced HF rats. The results showed that DSS-administrated rats resulted in decreasing in hepatosomatic indexes, and lowering serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST). Meanwhile, the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) were increased, while the content of malonaldehyde (MDA) was lessened in liver tissue of DSS administration group. In addition, the pro-fibrotic markers of hydroxyproline (Hyp), type III procollagen (PCIII) and hyaluronic acid (HA) contents were decreased. Histopathological examination confirmed that the hepatotoxicity in CCl4-injured rats was alleviated following the DSS administration. Furthermore, intrahepatic protein expressions of alpha-smooth muscle actin (α-SMA), phosphorylated JAK2 (p-JAK2) and phosphorylated STAT3 (p-STAT3) were effectively down-regulated, respectively. Overall, this work demonstrates that DSS played the protective effect against CCl4-induced cytotoxicity in liver tissue, which the probable mechanism is associated with attenuation of lipid peroxidation, collagen accumulation and enhancement of anti-oxidative defense capability, as well as regulation of intrahepatic JAK/STAT pathway for maintaining collagenic homoeostasis.

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来源期刊
Pathologie-biologie
Pathologie-biologie 医学-病理学
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6-12 weeks
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