| 内质网应激介导细胞凋亡在运动预防非酒精性脂肪肝形成中的作用 |
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| 引用本文： | 李军汉,苏全生,孙君志,彭丽文,谢红苑.内质网应激介导细胞凋亡在运动预防非酒精性脂肪肝形成中的作用[J].北京体育大学学报,2015,38(10):58-62+108. |
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| 作者姓名： | 李军汉 苏全生 孙君志 彭丽文 谢红苑 |
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| 作者单位： | 成都体育学院，四川 成都 610041；北京体育大学，北京 100084,成都体育学院，四川 成都 610041,成都体育学院，四川 成都 610041,成都体育学院，四川 成都 610041,成都体育学院，四川 成都 610041 |
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| 基金项目： | 基金项目：“十二五”国家科技支撑计划重点项目子课题(2012BAK21B01-4)；四川省科技厅应用基础计划项目（2015JY0155）。 |
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| 摘 要： | 摘要：目的：探讨运动对非酒精性脂肪肝（NAFLD）的预防作用及作用机理。方法： SD雄性大鼠随机分为对照组、模型组和运动组3 组。对照组给予普通饲料喂养，模型组予高脂饲料喂养，运动组在高脂饲料喂养的同时予运动干预，连续8周，直至实验结束。HE染色观察肝脏病理形态变化，TUNEL法测肝细胞凋亡，western blot检测CHOP、Caspase12和JNK蛋白表达，免疫组化检测CHOP、Caspase12和JNK蛋白阳性表达。结果：1）与对照组比较，模型组肝细胞脂肪性变明显，肝细胞凋亡指数升高，CHOP、Caspase12、JNK蛋白表达及阳性表达增加；2）与模型组比较，运动组肝细胞脂肪变性减轻，肝细胞凋亡指数减少，CHOP、Caspase12、JNK蛋白表达及阳性表达降低。结论：8周高脂饮食可成功复制NAFLD动物模型，内质网应激介导细胞凋亡参与NAFLD形成。运动对NAFLD形成具有较好的预防作用，其机制可能与运动可降低内质网应激介导细胞凋亡蛋白CHOP、JNK和Caspase12在肝细胞的表达，抑制肝细胞凋亡有关。
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| 关 键 词： | 关键词：内质网应激 非酒精性脂肪肝 细胞凋亡 游泳运动 NAFLD动物模型 |
| 收稿时间： | 2015/6/18 0:00:00 |
Effects of Exercise on Endoplasmic Reticulum Stress Induced Apoptosis of Liver Cells in Rats with Non-alcoholic Fatty Liver Diseases Model |
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| LI Jun-han,SU Quan-sheng,SUN Jun-zhi,PENG Li-wen and XIE Hong-yuan.Effects of Exercise on Endoplasmic Reticulum Stress Induced Apoptosis of Liver Cells in Rats with Non-alcoholic Fatty Liver Diseases Model[J].Journal of Beijing Sport University,2015,38(10):58-62+108. |
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| Authors: | LI Jun-han SU Quan-sheng SUN Jun-zhi PENG Li-wen and XIE Hong-yuan |
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| Institution: | Chengdu Sport University, Chengdu 610041, Sichuan China; Beijing Sport University, Beijing 100084, China,Chengdu Sport University, Chengdu 610041, Sichuan China,Chengdu Sport University, Chengdu 610041, Sichuan China,Chengdu Sport University, Chengdu 610041, Sichuan China and Chengdu Sport University, Chengdu 610041, Sichuan China |
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| Abstract: | Abstract: Objective: The purpose of study was to explore the effects and intervention mechanism of exercise on nonalcoholic fatty liver disease. Methods: SD rats were randomly divided into control group, model group and exercise group. Control group were fed with ordinary diet, model group were fed with high-fat diet, exercise group underwent 8 weeks aerobic exercise and were fed with high-fat diet. Pathological change of liver tissue was observed after HE staining, apoptosis of liver was observed by terminal-deoxynucleoitidyl terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL), the protein expressions of CHOP, Caspase-12 and JNK were tested by Western blotting and Immunohistochemistry. Results: 1) Compared with control group, hepatocyte steatosis is aggravating and liver cell apoptosis index increases and protein expressions of CHOP and Caspase12 and JNK increase in model group; 2) Compared with model group, liver steatosis is alleviated and liver cell apoptosis decreases and the protein expressions of CHOP and Caspase12 and JNK decrease in exercise group. Conclusions: Eight weeks high fat diet could successfully establish the model of rat with nonalcoholic fatty liver disease. Exercise has a good preventive effect on non-alcoholic fatty liver disease, which may be related to the decrease of the protein expressions of CHOP, JNK and Caspase12 that reduced liver cell apoptosis. |
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| Keywords: | Keywords: endoplasmic reticulum stress non-alcoholic fatty liver disease cell apoptosis swimming NAFLD model |
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