【摘要】 目的了解VitE和硒联合干预对急性肝损伤期肝星形细胞增殖和凋亡的影响。方法采用腹腔内注射50%CCl4制备大鼠急性肝损伤模型,在饲料中添加适量VitE(250mg/kg饲料)和硒(0.2mg/kg饲料)进行营养干预,分别在第1次和第3次注射CCl4后的6、24、48、72h处死大鼠,取其肝组织,用αSMA免疫组化方法检测激活的HSC细胞,用原位凋亡(TUNEL)技术和αSMA免疫组化双标染色检测HSC凋亡。结果注射CCl4后HSC激活,并在第1次注射后72h活化HSC数量达到高峰;在所观察的各时间点,随时间延长HSC凋亡数逐步增加;在同一时间点,抗氧化剂干预组HSC数量少于病理造模组。结论饲料中添加适量VitE和硒可抑制CCL4所致的急性期肝损伤时HSC的激活和(或)增殖,并促进激活的HSC凋亡。更多还原

【Abstract】 Objective To evaluate the effect of vitamin E and selenium on hepatic stellate cell (HSC) proliferation and apoptosis in acute liver injury. Methods We built the rat model of acute liver damage induced by intra- peritoneal injection with CCl 4. The rats from the intervention group were fed with chow supplemented with vitamin E (250 mg/kg) and selenium (0.2 mg/kg), and the others were given standard chow. Activatd HSC was determined by α-smooth muscle actin immunohistochemistry staining and apoptotic HSC was determined by dual staining terminal deoxynucleotidyl transferase UTP nick end labeling (TUNEL) and α-smooth muscle actin immunohistochemistry. Results We found that, at 24 h after the first injection with CCl 4, the number of HSCs in the liver began to increase and got to the peak at 72 h, at the same times, the number of apoptotic HSCs also increased with the time point. At each time point, HSCs in intervention group were more than the pathological group. Conclusion Dietary supplement with proper vitamin E and selenium can inhibit the activation and/or proliferation of HSCs and promote the apoptosis of activated HSCs in acute damage induced by CCl 4.更多还原