Hepatic fibrosis is a pathological change that is a major problem in chronic liver disease. As an important biologically active substance, the Aronia melanocarpa Elliot anthocyanins (AMA) has a strong anti-oxidation property and may have certain preventive and therapeutic effects on hepatic fibrosis diseases. The current research was designed for evaluation the antifibrotic effects and mechanism of AMA on CCl₄-induced liver injury in mice. Mice injected with CCl₄ twice a week at the same time as treated with 20 or 40 mg/kg AMA by gavage every day. After 8 weeks, biochemical parameters were used to estimate liver damage, such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and total serum bilirubin (TSB), total protein (TP) and albumin (ALB). In addition, oxidative stress parameters such as superoxide dismutase (SOD) and reduced glutathione (GSH) were also studied. And the role of TNF-α, IL-1, IL-6, COX-2 as markers of inflammation at the transcriptional level. Histopathological examination of liver tissue was performed and compared to controls. Collagen I, alpha smooth muscle actin (α-SMA), transforming growth factorβ1 (TGF-β1) and SMAD2 were also evaluated as markers of fibrosis. The results showed that AMA improved CCl₄-induced fibrosis, such as histopathological scores, markers of liver damage and oxidative stress. In addition, we investigated the potential mechanisms of underlying these effects, including: (1) inhibiting fibrosis by reducing the expression of inflammatory factors such as TNF-α and IL-1; (2) Prevent liver fibrosis by inactivating α-SMA expression; (3) inhibition of TGF-β1 secretion and Collagen I deposition to down-regulate the fiber reaction of HSC. In conclusion, this study illustrated the anti-fibrotic effects of AMA and may be a new candidate for the treatment of hepatic fibrosis.

肝纤维化是一种病理变化，是慢性肝病的主要问题。作为一种重要的生物活性物质，黑木阿罗尼亚花青素（AMA）具有很强的抗氧化性能，并且可能对肝纤维化疾病具有一定的预防和治疗作用。本研究旨在评估AMA对CCl ₄诱导的小鼠肝损伤的抗纤维化作用及其机制。注射CCl _4的小鼠每周两次，每天两次，每天20或40 mg / kg AMA进行管​​饲。8周后，使用生化参数评估肝脏损伤，例如天冬氨酸转氨酶（AST），丙氨酸转氨酶（ALT），碱性磷酸酶（ALP）和总血清胆红素（TSB），总蛋白（TP）和白蛋白（ALB） ）。此外，还研究了氧化应激参数，如超氧化物歧化酶（SOD）和还原型谷胱甘肽（GSH）。TNF-α，IL-1，IL-6，COX-2在转录水平上是炎症的标志物。进行肝组织的组织病理学检查并将其与对照进行比较。胶原I，α平滑肌肌动蛋白（α-SMA），转化生长因子β1（TGF-β1）和SMAD2也被评估为纤维化的标志物。结果表明AMA改善了CCl ₄-诱导的纤维化，例如组织病理学评分，肝损伤和氧化应激的标志物。此外，我们研究了潜在的潜在作用机制，包括：（1）通过减少炎症因子如TNF-α和IL-1的表达抑制纤维化；（2）通过使α-SMA表达失活来预防肝纤维化；（3）抑制TGF-β1的分泌和I型胶原的沉积，从而下调HSC的纤维反应。总而言之，这项研究说明了AMA的抗纤维化作用，可能是治疗肝纤维化的新方法。