He Ya-jun, Shu Jian-chang, Lü Xia, Fang Li, Sheng Yan
Guangzhou Red Cross Hospital, Jinan University Medical Collage, Guangzhou 510220, China.
Zhonghua Gan Zang Bing Za Zhi. 2006 May;14(5):337-40.
To observe the prophylactic effect of curcumin on hepatic fibrosis and the number, location, apoptosis of activated hepatic stellate cells (HSCs) in the livers and to discuss the relationship between the prophylactic effects and activated HSC.
A rat model of hepatic fibrosis was established by intraperitoneal injection of carbon tetrachloride. Curcumin doses of 5 mg, 10 mg, 20 mg per 100 gram per 100g of body weight were given to three groups of the model rats. No curcumin was given to one group of the model rats and it served as the control. After eight weeks, all rats were sacrificed and their left liver lobes were examined histopathologically with H.E and Masson stainings. Grades of hepatic fibrosis were evaluated according to the SSS system. Activated HSC was detected by the alpha-SMA immunohistochemistry staining. HSC apoptosis was detected by double-stainings of terminal deoxynucleotidyl transferase (TdT) dUTP nick-end labeling (TUNEL) and desmin immunohistochemistry staining.
Degrees (SSS system scores) of hepatic fibrosis in the curcumin groups were all less severe in comparison with those of the control group. Activated HSCs in the livers of the rats of the control group increased significantly compared with that of the treatment groups, and also fewer apoptotic HSCs were detected in the control group. On the contrary, fewer activated HSCs and more apoptotic HSCs were detected in the curcumin groups compared with those of the control group. The degrees of the effects were curcumin dose-dependent.
Curcumin can prevent hepatic fibrosis. It can inhibit activation and proliferation of HSCs and induce HSCs apoptosis, which may be the mechanism(s) contributing to the prophylactic effects of curcumin on hepatic fibrosis.
观察姜黄素对肝纤维化的预防作用以及肝脏中活化肝星状细胞（HSCs）的数量、位置和凋亡情况，并探讨预防作用与活化HSC之间的关系。
通过腹腔注射四氯化碳建立大鼠肝纤维化模型。将三组模型大鼠分别给予每100克体重5毫克、10毫克、20毫克的姜黄素剂量。一组模型大鼠不给予姜黄素作为对照。八周后，处死所有大鼠，取其左肝叶进行苏木精-伊红（H.E）和Masson染色的组织病理学检查。根据SSS系统评估肝纤维化分级。通过α-SMA免疫组织化学染色检测活化的HSC。通过末端脱氧核苷酸转移酶（TdT）介导的dUTP缺口末端标记（TUNEL）与结蛋白免疫组织化学双染色检测HSC凋亡。
与对照组相比，姜黄素组的肝纤维化程度（SSS系统评分）均较轻。对照组大鼠肝脏中活化的HSC较治疗组显著增加，且对照组中检测到的凋亡HSC较少。相反，与对照组相比，姜黄素组中活化的HSC较少，凋亡的HSC较多。作用程度呈姜黄素剂量依赖性。
姜黄素可预防肝纤维化。它能抑制HSCs的活化和增殖并诱导HSCs凋亡，这可能是姜黄素对肝纤维化具有预防作用的机制。
