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目的探讨神经生长因子(NGF)在糖尿病周围神经病(DNP)发病中的作用以及醛糖还原酶抑制剂(ARI)改善生理功能和NGF水平的作用机制。方法采用链脲佐菌素(STZ)制成大鼠DNP模型后给予ARI治疗,检测大鼠治疗前后摇尾阈值、神经电生理和血清及坐骨神经NGF水平,并与DNP模型组和健康对照组相比较。结果与健康对照组比较,DNP模型大鼠摇尾阈值升高[(49.56±0.32)℃ vs.(47.60±1.37)℃,P<0.05],运动神经传导速度(MNCV)和感觉神经传导速度(SNCV)均下降[(32.82±2.96)m/s vs.(52.76±6.52)m/s,P<0.05;(39.22±8.15)m/s vs.(45.33±8.21)m/s,P<0.05],血清和坐骨神经中NGF水平下降[分别为(154.82±136.18)pg/mL vs.(313.71±156.99)pg/mL,P<0.05;(457.40±187.59)pg/mL vs.(688.93±1 6 7.85)pg/mL,P<0.05]。经ARI治疗后大鼠摇尾阈值显著低于DNP模型组(P<0.05),SNCV、血清及坐骨神经中NGF水平均显著高于DNP模型组(P<0.05),同时经ARI治疗后其摇尾阈值较治疗前显著降低,SNCV、MNCV较治疗前显著增高(P<0.05)。结论 NGF表达或运输水平下降在DNP发病中具有作用。ARI可促进NGF的表达并改善热痛觉和神经传导速度。
Objective To investigate the role of nerve growth factor (NGF) in the pathogenesis of diabetic peripheral neuropathy (DNP) and the mechanism by which aldose reductase inhibitor (ARI) improves the physiological function and NGF level. Methods The rat model of DNP was induced by streptozotocin (STZ), then the rats were given ARI to establish the rat model of DNP. The threshold, neuroelectrophysiology and serum NGF level of sciatic nerve were measured before and after treatment. The DNP model group and healthy control group Compare Results Compared with the healthy control group, the DNP model rats had higher tail-motion threshold (49.56 ± 0.32 ℃ vs. 47.60 ± 1.37 ℃, P <0.05), motor nerve conduction velocity (MNCV) and sensory nerve conduction velocity (P <0.05); (39.22 ± 8.15) m / s vs. (45.33 ± 8.21) m / s, P <0.05 ], And decreased NGF levels in serum and sciatic nerve [(154.82 ± 136.18) pg / mL vs. (313.71 ± 156.99) pg / mL, respectively; P <0.05 vs. (457.40 ± 187.59) pg / mL vs. (688.93 ± 16 7.85) pg / mL, P <0.05]. After ARI treatment, the threshold of rat tail-shaking was significantly lower than that of DNP model group (P <0.05). The levels of NGF in SNCV, serum and sciatic nerve were significantly higher than those in DNP model group (P <0.05) Thresholds were significantly lower than before treatment, SNCV, MNCV was significantly higher than before treatment (P <0.05). Conclusions The decrease of NGF expression or transport level plays a role in the pathogenesis of DNP. ARI promotes the expression of NGF and improves thermal pain and nerve conduction velocity.