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目的:研究高压氧治疗(HBOT)是否可改善STZ糖尿病大鼠的周围神经病变并探讨其机制。方法:将链脲佐菌素(STZ)糖尿病大鼠随机分为2组。HBOT组(n=31):每天接受0.15MPaHBOT1h,连续20天。糖尿病组(n=32):不做治疗。正常组(n=20):正常SD大鼠。分别在疗程10天、20天时测定右后肢胫神经、腓神经的传导速度(NCV)后处死治疗组及同期对照组大鼠,取动脉血用ELISA法和硝酸还原酶法测定3组血清NGF、IGF-1、NO和MMP-1水平。结果:治疗前糖尿病大鼠的胫腓神经的NCV明显低于正常组。HBO治疗10d后,治疗组后肢胫神经和腓神经的传导速度明显高于同期糖尿病组(P<0.05),但低于正常组;血清MMP-1水平明显降低,血清NGF、NO水平稍有增高,但与糖尿病组比较差异无显著性意义。20d后,治疗组后肢神经的传导速度明显高于同期糖尿病组(P<0.01),而与正常组间差异无显著性意义(P>0.05);治疗组雪旺细胞数明显增多,超微结构的异常如神经髓鞘纤维化增厚、轴索缩小变性等得到明显改善;血清NGF和NO水平显著高于糖尿病组(P<0.01),治疗组血IGF-1水平显著高于糖尿病组(P<0.001)。结论:HBOT可改善STZ大鼠糖尿病性周围神经病变,其机制可能与促进NGF、IGF-1、NO合成,抑制MMP-1有关。
Objective: To investigate whether hyperbaric oxygen therapy (HBOT) can improve peripheral neuropathy in STZ diabetic rats and to explore its mechanism. Methods: The streptozotocin (STZ) diabetic rats were randomly divided into two groups. HBOT group (n = 31): 0.15MPaHBOT1h daily for 20 consecutive days. Diabetes group (n = 32): No treatment. Normal group (n = 20): Normal SD rats. The tibial nerve and peroneal nerve conduction velocity (NCV) of the right hindlimb were measured at 10 days and 20 days after treatment respectively. The rats in the treatment group and the control group were sacrificed at the 10th and 20th days of treatment. The serum levels of NGF, IGF-1, NO and MMP-1 levels. Results: The NCV of tibiofibular nerve in pretreatment diabetic rats was significantly lower than that in normal rats. After 10 days HBO treatment, the conduction velocity of tibial nerve and peroneal nerve of hindlimb in treatment group was significantly higher than that in the same period of diabetic group (P <0.05), but lower than that in normal group. The serum MMP-1 level was significantly lower and serum NGF and NO levels were slightly increased , But no significant difference with the diabetic group. After 20 days, the conduction velocity of the hindlimb nerve in treatment group was significantly higher than that in the same period of diabetes group (P <0.01), but there was no significant difference between the two groups (P> 0.05). The number of Schwann cells in the treatment group was significantly increased, (P <0.01). The level of serum IGF-1 in the treatment group was significantly higher than that in the diabetic group (P <0.01). The levels of NGF and NO in the serum were significantly higher than those in the diabetic group <0.001). Conclusion: HBOT can improve diabetic peripheral neuropathy in STZ rats. The mechanism may be related to promoting the synthesis of NGF, IGF-1, NO and inhibiting the expression of MMP-1.