Protective effects of hydroxysafflor yellow A (HSYA) on alcohol-induced liver injury in rats
Protective effects of hydroxysafflor yellow A (HSYA) on alcohol-induced liver injury in rats
复制标题
羟基红花黄色素A（HSYA）对大鼠酒精性肝损伤的保护作用
DOI：
10.1007/s13105-015-0382-3
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发表时间：
2015-03-01
影响因子：
3.4
通讯作者：
Lin, Rong
中科院分区：
文献类型：
--
作者：
He, Yanhao;Liu, Qiang;Lin, Rong
羟基红花黄A （hydroxyysafflor yellow A， HSYA）是从红花中提取的主要天然活性成分。，已广泛用于治疗脑血管和心血管疾病。本研究旨在探讨HSYA对酒精性肝损伤的影响及其机制。采用雄性Sprague-Dawley大鼠建立酒精性肝损伤模型。HSYA通过降低大鼠丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、透明质酸（HA）、层粘连蛋白（LN）和III型前胶原（III- c）水平，改善血清生化指标。与模型组相比，HSYA能有效提高大鼠肝组织超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GPx）的活性和信使RNA (mRNA)，而酒精能明显降低这种活性。与模型组相比，HSYA还能明显降低大鼠肝组织中活性氧（ROS）和丙二醛（MDA）的水平，且酒精的作用明显增强。组织学研究表明，HSYA显著减少了大、微泡性脂肪变性的数量，抑制了肝纤维化，缩小了肝水肿变性区，改善了长期饮酒引起的肝损伤的严重程度，最终改善了肝脏的结构。此外，免疫组化研究表明，HSYA可显著阻断酒精刺激大鼠肝组织中转化生长因子β1 （TGF-β1）的激活。综上所述，HSYA能有效保护大鼠肝脏免受长期酒精损伤，其作用与增强肝组织抗氧化能力、抑制TGF-β1表达有关。
Hydroxysafflor yellow A (HSYA), the main active natural constituent extracted fromCarthamus tinctoriusL., has been widely used for the treatment of cerebrovascular and cardiovascular diseases. The aim of this study is to explore the effect of HSYA on alcohol-induced liver injury and the underlying mechanism. Male Sprague-Dawley rats were used to establish the liver injury model induced by alcohol. HSYA treatment ameliorated serum biochemical indicators by reducing the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), hyaluronan (HA), laminin (LN), and type III precollagen (III-C) in rats. HSYA efficiently increased the activity and messenger RNA (mRNA) of superoxide dismutase (SOD) and glutathione peroxidase (GPx) in rat liver tissue compared with those of model group, which was obviously reduced by alcohol. HSYA also apparently decreased the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) in rat liver tissue compared with those of model group, which was obviously enhanced by alcohol. Histological studies demonstrated that HSYA substantially reduced the number of macro- and micro-vesicular steatosis, suppressed hepatic fibrogenesis and shrunk ballooning degeneration areas, ameliorated the severity of liver damage induced by long-term drinking, and finally improved the liver architecture. In addition, immunohistochemistry study indicated that the activation of transforming growth factor β1 (TGF-β1) stimulated by alcohol in rat liver tissue was significantly blocked by HSYA. Collectively, these data demonstrated that HSYA can effectively protect the liver of rats from long-term alcohol injury, which relates with the enhanced antioxidant capacity of liver tissues and inhibition of TGF-β1 expression.