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针刺对高脂饮食肾损伤大鼠过氧化物酶增殖体活化受体γ蛋白表达的影响
引用本文:侯慧芳,王永玲,孟 莉,高建芝.针刺对高脂饮食肾损伤大鼠过氧化物酶增殖体活化受体γ蛋白表达的影响[J].新乡医学院学报,2014(3):179-181,186.
作者姓名:侯慧芳  王永玲  孟 莉  高建芝
作者单位:[1]新乡医学院基础医学院病理生理学教研室,河南新乡453003 [2]新乡医学院基础医学院生理学与神经生物学教研室,河南新乡453003 [3]新乡医学院法医学系法医综合实验室,河南新乡453003
基金项目:河南省教育厅资助项目(编号:2008831005);新乡医学院高学历资助项目(编号:04GXLP06)
摘    要:目的观察针刺对高脂饮食肾损伤大鼠过氧化物酶增殖体活化受体γ(PPAPγ)蛋白表达及肾细胞凋亡的影响。方法 50只SD大鼠随机分为正常组(n=10)和高脂组(n=40),高脂组建立高脂饮食肾损伤大鼠模型,再随机分为模型组(n=10)和针刺组(n=10),针刺组大鼠取足三里穴、内庭穴和天枢穴行针刺治疗,模型组大鼠不做治疗,14 d后处死,苏木精-伊红染色法观察模型组和针刺组大鼠肾组织形态学变化,免疫组织化学法检测肾组织PPARγ蛋白表达变化,原位末端转移酶标记法检测肾细胞凋亡情况,并与正常组大鼠进行比较。结果正常组大鼠肾脏正常皮质结构存在,未见髓质结构;模型组大鼠有个别肾小球内毛细血管局灶性玻璃样变性,近曲小管肿胀、变性、空泡形成,肾间质可见大量炎性细胞浸润;针刺组大鼠仍可见肾小管上皮细胞玻璃样变性,与模型组大鼠相比,肾小球内毛细血管玻璃样变性减少,肾小管上皮细胞空泡变性显著减少。与正常组大鼠比较,针刺组肾组织PPARγ蛋白表达无显著变化(P>0.05),而模型组大鼠肾组织PPARγ蛋白表达显著降低(P<0.05);针刺组大鼠肾组织PPARγ蛋白表达与模型组比较显著升高(P<0.05)。与正常组比较,模型组和针刺组大鼠的肾细胞凋亡指数均显著升高(P<0.05),但针刺组大鼠肾细胞凋亡指数与模型组比较显著降低(P<0.05)。结论针刺可能通过提高大鼠PPARγ蛋白表达,抑制肾细胞凋亡,减轻高脂饮食对肾脏的损伤。

关 键 词:针刺  高脂血症  过氧化物酶增殖体活化受体γ  凋亡

Effect of acupuncture on expression of peroxisome proliferator-activited recaptor gamma in rats with renal injury induced by high fat diet
HOU Hui-fang,WANG Yong-ling,MENG Li,GAO Jian-zhi.Effect of acupuncture on expression of peroxisome proliferator-activited recaptor gamma in rats with renal injury induced by high fat diet[J].Journal of Xinxiang Medical College,2014(3):179-181,186.
Authors:HOU Hui-fang  WANG Yong-ling  MENG Li  GAO Jian-zhi
Institution:1. Department of Pathophysiology,School of Basic Medicine ,Xinxiang Medical University,Xinxiang 453003, Henan Province, China ;2. Department of Physiology and Neurobiology , School of Basic Medicine, Xinxiang Medical University, Xinxiang 453003, Henan Province, China;3. Complex Laboratory of Forensic Medicine, School of Forensic Medicine, Xinxiang Medical University, Xinxiang 453003, Henan Province, China)
Abstract:Objective To explore the effect of acupuncture on the expression of peroxisome proliferator-activited recaptor gamma (PPARγ) and renal cell apoptosis in rats with renal injury induced by high fat diet. Methods Fifty Sprague-Dawley rats were radomly devided into nomal group ( n = 10 ) and high fat group ( n = 40 ). Animal model of renal injury rats induced by high fat diet was established in high fat group. And those rats were randomly assigned into model group( n = 10 ) and acupuncture group( n = 10). The acupuncture group was acupunctured "zusanli" ," neiting" and "tianshu" while the model group were not acupunetured. These rats were all killed after 14 days. After the treatment,the changes of kidney were observed by hematoxylin-eosin staining. The expression of PPARγ was analyzed by immunohistochemistry method. Renal cell apoptosis was detected by terminal deoxynueleotidyl transferase-mediated dUTP nick end labeling. These indexes above were compared with the those in normal group respectively. Results In the normal group, the renal cortical structure could be seen but the medul- lary structure couldn't be seen. In the model group, there were some glomerular capillaries with focal hyaline degeneration, some renal proximal tubule with swelling, degeneration, vacuolization. Many inflammatory cells were infiltrated in interstitial. Compared with the model group, the hyaline degeneration of renal tubular epithelial cells was still seen in the acupuncture group while other changes were lightened. Compared with the normal group, the expression of PPARγ had not changed in the acupuncture group (P 〉 0.05), while it was decreased in the model group ( P 〈 0.05). Compared with the model group, the ex- pression of PPARγincreased in the acupuncture group ( P 〈 0.05 ). Compared with the normal group, the index of renal cell apoptosis increased in both the model group and the acupuncture group(P 〈 0.05) while it decreased in the acupuncture group when compared with the model group(P 〈 0.05 ). Conclusion Acupuncture can lighten the injury of renal induced by high fat diet in rats though increasing the expression of PPARγand suppressing renal cell apoptosis.
Keywords:acupuncture  hyperlipidemia  peroxisome proliferator-activited recaptor gamma  apoptosis
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