乐果诱导的大鼠迟发性神经病神经营养因子变化的实验研究

Experimental study on NGF and GDNF of dimethoate induced delayed neurotoxicity in rats

目的探讨乐果所致迟发性神经毒性的神经营养因子的变化。方法建立乐果诱导的迟发性神经毒性的大鼠模型,免疫组化法检测神经生长因子(NGF)、胶质细胞源性神经营养因子(GDNF)在坐骨神经、脊髓及大脑叶皮质中的蛋白表达。结果实验4周时,低剂量组、高剂量组坐骨神经、腰骶膨大、大脑额叶皮质中的NGF、GDNF阳性目标积分光密度值均较对照组降低,差异有显著性(P<0·05)。结论乐果诱导的迟发性神经病表现为大脑、脊髓和坐骨神经中NGF、GDNF蛋白表达降低,在OPIDP早期给予NGF、GDNF治疗有其必要性的效性。

Objective To explore the changes of NGF,GDNF protein expression in the processiong of delayed polyneuropathy. Methods Established the rats OPIDP model induced by dimethoate. The sense function was measured by the tests of the tailflick threshold temperature. The protein expression of NGF and GDNF in ceredrum ,spain cord and sciatic nerve were analyzed by immunohistochemistry. Results Compared with the control group the area of probuction of positive reaction of NGF and GDNF in the sciatic nerve ,cortex of Frons and lumbosacral enlargement was dereased and there was significant difference （P〈0.05）. Conclusions The protein expression of NGF and GDNF in cerebrum ,spain cord and sciatic nerve decrease in the processiong of delayed polyneuropathy