AIM： To evaluate the effects of dietary supplementation with vitamin E and selenium on proliferation and apoptosis of hepatic stellate cells （HSCs）, in acute liver injury induced by CCI4, and to explore their role ...AIM： To evaluate the effects of dietary supplementation with vitamin E and selenium on proliferation and apoptosis of hepatic stellate cells （HSCs）, in acute liver injury induced by CCI4, and to explore their role in the recovery from hepatic fibrosis phase. METHODS： An acute liver damage model of rats was established by intraperitoneal injection of carbon tetrachloride （0.3 ml/100 g body weight） twice a week, then the rats were killed at 6, 24, 48, and 72 h after the first and third injection, respectively. A liver fibrosis model was established by the same injection for 8 wk. Then three rats were killed at 3, 7, 14, and 28 d after the last injection, respectively. 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 rats in the normal control group and pathological group were given standard chow. Livers were harvested and stained with hematoxylin and eosin, Sirius red. Activated HSCs were determined by s-smooth muscle actin immunohistochemistry staining. Apoptotic HSCs were determined by dual staining with the terminal deoxynucleotidyl transferase UTP nick end labeling （TUNEL） and α-smooth muscle actin immunohistochemistry. Serum alanine aminotransferase and aspartate aminotransferase were also analyzed. RESULTS： In the acute liver damage model, the degree of liver injury was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, while the number of apoptotic HSCs was more in the intervention group than in the pathological group. In the liver fibrosis model, the degree of liver fibrosis was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, and the number of apoptotic HSCs was more in the intervention group than in the pathological group. CONCLUSION： Vitamin E and selenium supplementation at the given level can inhibit CCI4-induced activation and proliferation of HSCs and promote the apoptosis of activated HSCs in acute damage phase. Vitamin E and selenium can also effectively decrease the degree of hepatic fibrosis and promote the recovery process.展开更多
AIM:To investigate the effect of vitamin E on oxidative stress status in the small intestine of diabetic rats. METHODS:Twenty-four male Wistar rats were randomly divided into three groups:Control (C),non-treated diabe...AIM:To investigate the effect of vitamin E on oxidative stress status in the small intestine of diabetic rats. METHODS:Twenty-four male Wistar rats were randomly divided into three groups:Control (C),non-treated diabetic (NTD) and vitamin E-treated diabetic (VETD) groups. The increases in lipid peroxidation,protein oxidation and superoxide dismutase (SOD) in these three groups was compared after 6 wk. RESULTS:There was no significant difference in catalase activity between NTD and control rats. Compared to NTD rats,the treatment with vitamin E significantly decreased lipid peroxidation and protein oxidation,and also increased catalase activity and SOD. CONCLUSION:The results revealed the occurrence of oxidative stress in the small intestine of diabetic rats. Vitamin E,as an antioxidant,attenuates lipid peroxidation and protein oxidation,and increases antioxidant defense mechanism.展开更多
文摘目的:探讨血管紧张素Ⅱ(AngⅡ)皮下灌泵诱导Apo E-/-小鼠建立腹主动脉瘤模型的特点和可行性。方法:选取8-10周龄雄性Apo E-/-小鼠,通过植入式微量渗透释放泵皮下泵入AngⅡ(1000 ng/kg·min),持续泵入28天;对照组小鼠泵入生理盐水28天。取材后,测量小鼠腹主动脉直径,固定包埋做石蜡切片进行HE及弹力纤维染色,用Real-time PCR方法检测腹主动脉中α-平滑肌肌动蛋白(α-SMA)和骨桥蛋白(OPN)的表达。结果:AngⅡ处理组小鼠成瘤率为80%,腹主动脉直径较生理盐水对照组明显增加(P<0.05);病理染色显示炎症细胞明显增多,弹力纤维断裂增多,胶原合成增多。小鼠腹主动脉α-SMA m RNA表达较对照组显著降低(P<0.05),而OPN m RNA表达较对照组明显增高(P<0.05)。结论:通过AngⅡ连续灌注28天可以诱导Apo E-/-小鼠发生腹主动脉瘤,腹主动脉平滑肌细胞由收缩型向分泌型转化可能作为小鼠腹主动脉瘤发生的鉴定及治疗靶点之一。
基金Supported by the Science Research Foundation of Ministry of Public Health of China, No. 98-2-280
文摘AIM： To evaluate the effects of dietary supplementation with vitamin E and selenium on proliferation and apoptosis of hepatic stellate cells （HSCs）, in acute liver injury induced by CCI4, and to explore their role in the recovery from hepatic fibrosis phase. METHODS： An acute liver damage model of rats was established by intraperitoneal injection of carbon tetrachloride （0.3 ml/100 g body weight） twice a week, then the rats were killed at 6, 24, 48, and 72 h after the first and third injection, respectively. A liver fibrosis model was established by the same injection for 8 wk. Then three rats were killed at 3, 7, 14, and 28 d after the last injection, respectively. 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 rats in the normal control group and pathological group were given standard chow. Livers were harvested and stained with hematoxylin and eosin, Sirius red. Activated HSCs were determined by s-smooth muscle actin immunohistochemistry staining. Apoptotic HSCs were determined by dual staining with the terminal deoxynucleotidyl transferase UTP nick end labeling （TUNEL） and α-smooth muscle actin immunohistochemistry. Serum alanine aminotransferase and aspartate aminotransferase were also analyzed. RESULTS： In the acute liver damage model, the degree of liver injury was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, while the number of apoptotic HSCs was more in the intervention group than in the pathological group. In the liver fibrosis model, the degree of liver fibrosis was more serious in the pathological group than in the intervention group. At each time point, the number of activated HSCs was less in the intervention group than in the pathological group, and the number of apoptotic HSCs was more in the intervention group than in the pathological group. CONCLUSION： Vitamin E and selenium supplementation at the given level can inhibit CCI4-induced activation and proliferation of HSCs and promote the apoptosis of activated HSCs in acute damage phase. Vitamin E and selenium can also effectively decrease the degree of hepatic fibrosis and promote the recovery process.
文摘AIM:To investigate the effect of vitamin E on oxidative stress status in the small intestine of diabetic rats. METHODS:Twenty-four male Wistar rats were randomly divided into three groups:Control (C),non-treated diabetic (NTD) and vitamin E-treated diabetic (VETD) groups. The increases in lipid peroxidation,protein oxidation and superoxide dismutase (SOD) in these three groups was compared after 6 wk. RESULTS:There was no significant difference in catalase activity between NTD and control rats. Compared to NTD rats,the treatment with vitamin E significantly decreased lipid peroxidation and protein oxidation,and also increased catalase activity and SOD. CONCLUSION:The results revealed the occurrence of oxidative stress in the small intestine of diabetic rats. Vitamin E,as an antioxidant,attenuates lipid peroxidation and protein oxidation,and increases antioxidant defense mechanism.
