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大鼠酒精性肝病细胞凋亡中Caspase-3、NF-κB的表达 被引量:4
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作者 崔香丹 金武丕 李香 《陕西医学杂志》 CAS 2009年第3期273-275,共3页
目的:观察大鼠酒精性肝病组织病理形态学改变,探讨细胞凋亡与Caspase-3、NF-κB的表达及意义。方法:采用灌胃法制备大鼠酒精性肝病(ALD)模型,模型组用40%酒精8g/(kg·d)分两次灌胃共12周,对照组灌等量的生理盐水,实验第8、12周末分... 目的:观察大鼠酒精性肝病组织病理形态学改变,探讨细胞凋亡与Caspase-3、NF-κB的表达及意义。方法:采用灌胃法制备大鼠酒精性肝病(ALD)模型,模型组用40%酒精8g/(kg·d)分两次灌胃共12周,对照组灌等量的生理盐水,实验第8、12周末分批处死动物。用HE染色和电镜分别观察肝组织病理变化和肝细胞超微结构变化,用TUNEL法检测肝细胞的凋亡,用免疫组化法检测Caspase-3、NF-κB的表达。结果:模型组肝细胞凋亡明显增多,主要分布在中央静脉周围,点状、灶状坏死区;Caspase-3、NF-κB主要分布在中央静脉及肝细胞坏死灶周围细胞的胞质中,模型组Caspase-3、NF-κB表达强度明显高于对照组,且NF-κB的表达与Caspase-3的表达呈正相关。结论:大鼠酒精性肝病的发生、发展过程中Caspase-3、NF-κB参与肝细胞凋亡。 展开更多
关键词 肝疾病 酒精性/免疫学 @Caspase-3 NF—κB/分析 细胞凋亡 大鼠
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Expression of p53,Bax and Bcl-2 proteins in hepatocytes in non-alcoholic fatty liver disease 被引量:48
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作者 Anatol Panasiuk Janusz Dzieciol +1 位作者 Bozena Panasiuk Danuta Prokopowicz 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第38期6198-6202,共5页
AIM: To analyze the protein expression essential for apoptosis in liver steatosis. METHODS: The expression of proapoptotic proteins p53, Bax, and antiapoptotic Bcl-2 in hepatocytes with steatosis (SH) and without stea... AIM: To analyze the protein expression essential for apoptosis in liver steatosis. METHODS: The expression of proapoptotic proteins p53, Bax, and antiapoptotic Bcl-2 in hepatocytes with steatosis (SH) and without steatosis (NSH) was evaluated in 84 patients at various stages of non-alcoholic fatty liver disease (NAFLD). RESULTS: Immunohistochemical staining of liver tissue showed the activation of p53 protein in SH and NSH with increased liver steatosis, diminished Bcl-2 and slightly decreased Bax protein. Positive correlation was found between the stage of liver steatosis with p53 expression in SH (r = 0.54, P < 0.01) and NSH (r = 0.49, P < 0.01). The antiapoptotic protein Bcl-2 was diminished together with the advancement of liver steatosis, especially in non-steatosed hepatocytes (r =0.43, P < 001). CONCLUSION: Apoptosis is one of the most important mechanisms leading to hepatocyte elimination in NAFLD. The intensification of inflammation in NAFLD induces proapoptotic protein p53 with the inhibition of antiapoptotic Bcl-2. 展开更多
关键词 Apoptosis Non-alcoholic liver disease P53 BCL-2 BAX IMMUNOHISTOCHEMISTRY
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Immunological response in alcoholic liver disease 被引量:9
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作者 Michael J Duryee Lynell W Klassen Geoffrey M Thiele 《World Journal of Gastroenterology》 SCIE CAS CSCD 2007年第37期4938-4946,共9页
The development of alcoholic liver disease (ALD) can be attributed to many factors that cause damage to the liver and alter its functions. Data collected over the last 30 years strongly suggests that an immune compone... The development of alcoholic liver disease (ALD) can be attributed to many factors that cause damage to the liver and alter its functions. Data collected over the last 30 years strongly suggests that an immune component may be involved in the onset of this disease. This is best evidenced by the detection of circulating autoantibodies, infiltration of immune cells in the liver, and the detection of hepatic aldehyde modified proteins in patients with ALD. Experimentally, there are numerous immune responses that occur when proteins are modified with the metabolites of ethanol. These products are formed in response to the high oxidative state of the liver during ethanol metabolism, causing the release of many inflammatory processes and potential of necrosis or apoptosis of liver cells. Should cellular proteins become modified with these reactive alcohol metabolites and be recognized by the immune system, then immune responses may be initiated. Therefore, it was the purpose of this article to shed some insight into how the immune system is involved in the development and/or progression of ALD. 展开更多
关键词 Alcoholic liver disease Liver endothelial cells Aldehyde adducts Oxidative stress Immune system CYTOKINES METABOLISM
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