Department of Toxicology, College of Pharmacy, Chungnam National University, Gung-dong, Daejeon, Republic of Korea.
Food Chem Toxicol. 2010 Nov;48(11):3137-43. doi: 10.1016/j.fct.2010.08.009. Epub 2010 Aug 20.
In current study, we investigated the protective effects of the anthocyanin fraction (AF) obtained from the purple-fleshed sweet potato on hepatic fibrosis induced by dimethylnitrosamine (DMN) administration in rats. Treatment with DMN for 4 weeks produced marked liver fibrosis as assessed by increased serum alanine aminotransferase and aspartate aminotransferase activity and hepatic collagen content. These increases were inhibited by treatment with AF prior to the administration of DMN. In addition, AF inhibited DMN-induced reductions in rat body and liver weights in a dose-dependent manner. Histopathological evaluation of the rat livers revealed that AF reduced the incidence of hepatic fibrosis lesions and inhibited DMN-induced increases in α-smooth muscle actin (α-SMA) and collagen type I and III expression levels. AF also decreased DMN-induced expression levels platelet-derived growth factor receptors-beta, tumor necrosis factor-alpha and transforming growth factor-beta. This study demonstrates that AF administration can effectively improve liver fibrosis caused by DMN, and may be used as a therapeutic option and preventive measure against hepatic fibrosis.
在当前的研究中,我们研究了从紫薯中提取的花色苷(AF)对二甲基亚硝胺(DMN)诱导的大鼠肝纤维化的保护作用。用 DMN 处理 4 周可导致血清丙氨酸氨基转移酶和天冬氨酸氨基转移酶活性以及肝胶原含量显著增加,从而评估肝纤维化。在用 DMN 处理之前,用 AF 处理可抑制这些增加。此外,AF 以剂量依赖性方式抑制 DMN 诱导的大鼠体重和肝重降低。对大鼠肝脏的组织病理学评估表明,AF 降低了肝纤维化病变的发生率,并抑制了 DMN 诱导的α-平滑肌肌动蛋白(α-SMA)和胶原 I 和 III 表达水平的增加。AF 还降低了 DMN 诱导的血小板衍生生长因子受体-β、肿瘤坏死因子-α和转化生长因子-β的表达水平。这项研究表明,AF 的给药可以有效改善 DMN 引起的肝纤维化,并且可以用作治疗肝纤维化的选择和预防措施。