中文摘要：

目的通过构建糖尿病周围神经病变（DPN）大鼠模型,观察DPN大鼠坐骨神经中内质网应激与凋亡相关蛋白表达变化,探讨内质网应激在DPN中的可能作用机制。方法取36只8周龄雄性Wistar大鼠,适应性饲养1周后,选取其中12只作为正常对照组（CON组）,其余24只通过高脂饮食结合腹腔注射链脲佐菌素（STZ）方法,将大鼠分别构建成糖尿病组（DM组,12只）、DPN组（12只）模型。造模成功后检测3组大鼠血糖与坐骨神经传导速度,并取大鼠坐骨神经,采用Western blotting方法检测内质网应激蛋白CHOP、PERK与凋亡相关蛋白Bax、Caspase-12、Bcl-2表达水平。结果与CON组比较,DM组血糖水平明显升高（P〈0.001）,运动神经传导速度明显减慢（P〈0.001）;内质网应激蛋白CHOP、PERK表达水平增加（P=0.003,P〈0.001）;促凋亡蛋白Bax、Caspase-12表达增加（P〈0.001,P〈0.001）,抗凋亡蛋白Bcl-2表达降低（P〈0.001）。与DM组比较,DPN组大鼠坐骨神经内质网应激蛋白CHOP、PERK表达水平增加（P〈0.001,P=0.01）,Bax、Caspase-12表达增加（P〈0.001,P=0.002）,Bcl-2表达水平降低（P〈0.001）。结论 DPN大鼠模型坐骨神经存在明显的内质网应激反应增加、凋亡上调,内质网应激参与了DPN的发生过程。

英文摘要：

Objective To observe endoplasmic reticulum stress（ ERS） and apoptosis-related protein in diabetic peripheral neuropathy（ DPN） in animal models and to investigate the possible mechanism. Methods A total of 36 Wistar rats were divided into 3 groups： control group（ n = 12,CON group）,diabetic mellitus group（ n = 12,DMgroup）,and diabetic peripheral neuropathy group（ n = 12,DPN group）. The blood glucose（ BG） and motor nerve conduction velocity（ MNCV） were measured. The proteins,including CHOP,PERK,Bax,Bcl-2 and Caspase-12 were determined with Western blotting. Results Compared with CON group,the DMgroup had greatly increased BG and significantly decreased MNCV（ both P 〈 0. 001）; higher expression of CHOP,PERK,Bax,and Caspase-12（ P = 0. 003,P 〈 0. 001,P 〈 0. 001,P 〈 0. 001）,but lower expression of Bcl-2（ P 〈 0. 001）. Compared with the DMgroup,the DPN group had elevated expression of CHOP,PERK,Bax,and Caspase-12（ P 〈 0. 001,P = 0. 001,P 〈 0. 001,P =0. 002）,but lower expression of Bcl-2（ P 〈 0. 001）. Conclusion In animal models of DPN,the ERS in sciatic nerve is increases,and the level of apoptosis also increases,indicating that ERS is involved in the occurrence of DPN.