Department of liver disease, Qingdao No.6 People's Hospital, Shandong Province, China.
Remote Consultation Center, Qingdao No.6 People's Hospital, Shandong Province, China.
Pharmacology. 2021;106(5-6):323-331. doi: 10.1159/000514594. Epub 2021 Mar 29.
Hepatic fibrosis is an inflammatory liver disease, and there is no effective therapy at present. Astilbin is a bioactive ingredient found in many medicinal and food plants, with antioxidative, anti-inflammatory, and antitumor properties.
This study aimed to investigate the protective effect and related molecular mechanism of astilbin against carbon tetrachloride (CCl4)-induced liver fibrosis in rats.
Liver fibrosis was induced by injection of CCl4 in male Sprague-Dawley rats, and those rats were then treated with astilbin at different concentrations. Pathological changes, collagen production, inflammatory cytokine, and oxidative stress were evaluated to evaluate the effects of astilbin on CCl4-induced hepatic fibrosis. Real-time PCR and western blot were performed to detect the mRNA and protein expression of indicated genes.
We discovered that CCl4 caused significant fibrosis damage in rat liver, and astilbin dose-dependently improved the liver functions and fibrosis degree. Astilbin treatment significantly decreased collagen production, inflammatory response, and oxidative stress in vivo. Mechanically, administration of astilbin obviously elevated the hepatic levels of Nrf2 and its downstream components, including NAD(P)H:quinone oxidoreductase 1 (Nqo1), heme oxygenase (HO-1), glutamate-cysteine ligase catalytic subunit, and glutamate cysteine ligase modifier.
Taken together, these findings demonstrate that astilbin could protect against CCL4 induced-liver fibrosis in rats.
肝纤维化是一种炎症性肝病，目前尚无有效的治疗方法。紫云英苷是许多药用和食用植物中的一种生物活性成分，具有抗氧化、抗炎和抗肿瘤特性。
本研究旨在探讨紫云英苷对大鼠四氯化碳（CCl4）诱导肝纤维化的保护作用及相关分子机制。
雄性 Sprague-Dawley 大鼠经 CCl4 注射诱导肝纤维化，然后用不同浓度的紫云英苷进行治疗。评估病理变化、胶原产生、炎症细胞因子和氧化应激，以评估紫云英苷对 CCl4 诱导的肝纤维化的影响。实时 PCR 和 Western blot 用于检测指示基因的 mRNA 和蛋白表达。
我们发现 CCl4 导致大鼠肝纤维化明显损伤，紫云英苷呈剂量依赖性改善肝功能和纤维化程度。紫云英苷治疗可显著降低体内胶原产生、炎症反应和氧化应激。在机制上，给予紫云英苷可明显提高肝脏中 Nrf2 及其下游成分的水平，包括 NAD(P)H：醌氧化还原酶 1（Nqo1）、血红素加氧酶（HO-1）、谷氨酰胺半胱氨酸连接酶催化亚基和谷氨酰胺半胱氨酸连接酶修饰酶。
综上所述，这些发现表明紫云英苷可预防 CCl4 诱导的大鼠肝纤维化。
