高压氧对糖尿病大鼠周围神经病变的改善作用及其机制

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目的:研究高压氧治疗是否可改善链脲佐菌素(streptozocin,STZ)糖尿病大鼠的周围神经病变并探讨其机制。方法:SD大鼠83只,用STZ制造糖尿病模型成功60d、肌电图和电镜证实有周围神经病变后,随机分为3组:①高压氧组n=31):每天接受(0.15MPa、高压氧1h,连续20d。②糖尿病对照组n=32):不做治疗。(③正常对照组(n=20):腹腔注射生理盐水的无糖尿病的正常STZ大鼠。分别在疗程5,10,20d时测定右后肢胫神经、腓神经的传导速度(nerveconductionvelocity,NCV和H反射后处死治疗组及同期对照组)大鼠,取坐骨神经进行苏木精-伊红染色病理学观察,同时进行电镜观察。结果:治疗前糖尿病大鼠的胫神经(28.56±6.99)mm/s、腓神经(28.92±7.37)mm/s的NCV明显低于正常组犤分别为(48.29±8.04)mm/s,(51.93±8.50)mm/s犦,而H反射的潜伏期延长,波幅变小。高压氧治疗10d后,治疗组后肢胫神经(45.17±9.80)mm/s和腓神经的传导速度(43.81±7.05)mm/s明显高于同期糖尿病对照组,但低于正常对照组;治疗组H反射的潜伏期(7.27±0.76)ms较糖尿病对照组(7.49±1.26)ms缩短,波幅增大1.09±0.39)mV,(0.57±0.30)mV,犤(P<0.05犦;病理学变化不明显,但电镜观察显示治疗组的许旺细胞数较糖尿病对照组增多,髓鞘结构有所改善;氧疗20d后,治疗组后肢胫神经? Objective: To investigate whether hyperbaric oxygen therapy can improve the peripheral neuropathy of streptozocin (STZ) diabetic rats and explore its mechanism. Methods: Totally 83 SD rats were treated with STZ for 60 days. The electrocardiogram and electron microscopy were used to confirm the presence of peripheral neuropathy. The rats were randomly divided into three groups: ① hyperbaric oxygen group (n = 31) Oxygen 1h, continuous 20d. ② diabetic control group n = 32): do not make treatment. Normal control group (n = 20): Normal STZ rats without diabetes mellitus were injected intraperitoneally with normal saline.The nerve conduction velocity of the tibial nerve and peroneal nerve were measured at 5, 10 and 20 days of treatment (NCV and H The rats in the treatment group and the control group after reflex were sacrificed and the sciatic nerve was harvested for hematoxylin-eosin staining and electron microscopy.Results: The tibial nerve (28.56 ± 6.99) mm / s (48.29 ± 8.04) mm / s, (51.93 ± 8.50) mm / s, respectively, in the peroneal nerve (28.92 ± 7.37) mm / s, while the latency of H reflex was longer and the amplitude was smaller After hyperbaric oxygen treatment for 10 days, the tibial nerve (45.17 ± 9.80) mm / s and the peroneal nerve conduction velocity (43.81 ± 7.05) mm / s in the treatment group were significantly higher than those in the control group but lower than those in the normal control group Compared with diabetic control group (7.49 ± 1.26) ms, the latency of group H reflex (7.27 ± 0.76) ms was 1.09 ± 0.39 mV, (0.57 ± 0.30) mV, (P <0.05); pathological changes were not Obviously, however, electron microscopy showed that the number of Schwann cells in the treatment group increased compared with the diabetic control group and the myelin structure was improved. After 20 days of oxygen therapy, the treatment group Limb tibial nerve?
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