氧化应激对糖尿病大鼠Neuritin水平和坐骨神经功能及超微结构的影响

Effects of oxidative stress on neuritin level,sciatic nerve function and ultrastructure in rats with diabetes

目的探讨氧化应激对糖尿病大鼠血清Neuritin水平和坐骨神经功能及超微结构的影响。方法 40只SD大鼠随机均分为四组。NC组作为空白对照;DC、LD和HD组大鼠腹腔注射链脲佐菌素55mg/kg建立糖尿病模型。DC组为模型对照;LD和HD组分别腹腔注射硫辛酸20mg·kg-1·d-1和40mg·kg-1·d-1,连续用药6周。分别在给药2、4、6周时检测大鼠血清丙二醛(MDA)、Neuritin的含量及超氧化物歧化酶(SOD)的活性,测量坐骨神经运动传导速度(MNCV),采用透射电镜观察坐骨神经超微结构。结果与NC组相比,DC组2周后MDA含量升高,SOD活性和Neuritin含量降低(P<0.05),4周后坐骨神经MNCV降低(P<0.05),坐骨神经出现脱髓鞘病变。与DC组相比,LD、HD组给药2周后SOD活性和Neuritin含量升高(P<0.05),给药4周后MDA含量降低,坐骨神经MNCV升高(P<0.05)。结论氧化应激可能直接或者通过影响Neuritin水平引起糖尿病外周神经的异常。

Objective To investigate the effects of oxidative stress on serum level of neuritin, sciatic nerve function and ultrastructure in rats with diabetes. Methods A total of 40 SD male rats was equally and randomly divided into 4 groups. The rats in group NC were taken as blank controls. Rat models with diabetes were established by intraperitoneally injection of streptozotocin 55 mg/kg in groups of DC（model control）, LD and HD. The rats in groups of LD and HD were intraperitoneally injected with lipoic acid 20 mg · kg-1 · d^-1 and lipoic acid 40 mg · kg^-1 · d^-1 for 6 weeks. Serum levels of methane dicarboxylic aldehyde（MDA） and neuritin and activity of superoxide dismutase（SOD） were detected, motor nerve conduction velocity （MNCV） of sciatic nervesI was measured, and ultrastructure of sciatic nerves was observed by transmission electron microscope in 2,4 and 6 weeks I during treatment with lipoic acid. Results Compared with group NC, serum MDA was increased,SOD activity and neuritin level were decreased in 2 weeks during treatment（P〈0. 05）, and MNCV was decreased and axonal degeneration and demyelination of sciatic nerves were observed in 4 weeks during treatment in group DC（P〈0. 05）. Compared with group DC, SOD activity and neuritin level were increased in 2 weeks during treatment（P〈0. 05）, and serum MDA was decreased while MNCV was increased in 4 weeks during treatment in groups of LD and HD（P〈0. 05）. Conclusion Oxidative stress induces diabetic peripheral neuropathy directly or via affecting neuritin level.