【摘要】 目的　进一步探讨氯丙烯所致中毒性周围神经病的发病机制。方法　Wistar雄性大鼠sc氯丙烯3个月后 ,用Western印迹方法分别测定了氯丙烯亚慢性中毒后大鼠大脑、脊髓、坐骨神经沉淀和上清中骨架蛋白 β 肌动蛋白含量的变化。 结果　①在大脑沉淀中 ,β 肌动蛋白含量在氯丙烯 85 mg·kg- 1组降低 10 % (P >0 .0 5 ) ,170mg·kg- 1组降低 13% (P <0 .0 5 ) ;在大脑上清中 ,β 肌动蛋白含量在 85mg·kg- 1组降低 2 0 % (P <0 .0 1) ,170mg·kg- 1组无明显变化。②在脊髓沉淀中 ,氯丙烯 85mg·kg- 1组 β 肌动蛋白含量降低 13% ,170mg·kg- 1组降低 12 % ,但均无显著性差异 ;上清中无显著变化。③坐骨神经沉淀中 ,在氯丙烯 85和 170mg·kg- 1组分别下降33%和 39% (P <0 .0 1) ;上清中 ,β 肌动蛋白没有显著性变化。结论　首次发现氯丙烯可导致神经组织中β 肌动蛋白含量显著降低 ,β 肌动蛋白的改变可能与氯丙烯引起的中毒性外周神经病有关更多还原

【Abstract】 AIM In further explore the mechanism of allyl chloride(AC) induced occupational peripheral neuropathy. METHODS Thirty Wistar male rats were treated by sc AC 85 (low dose group) and 170 mg·kg-1 (high dose group) 5 d a week for 3 months, and the percent content changes of β actin in cerebrums, spinal cords and sciatic nerves were analyzed by Western blotting. RESULTS ① In cerebrum precipitant, β actin was decreased in high dose group (P<0.05) by 13%, while in supernatant only low dose group was observed such decrease(P<0.01) by 20%. ② In spinal cord precipitant and supernatant, no obvious change was observed. ③ In sciatic nerve, it could be found β actin reduced significantly both in low and high dose group precipitant (P<0.01), by 33% and 39%, respectively, but no remarkable changes in supernatant. CONCLUSION It is the first time that β actin contents are found disturbed in peripheral neuropathy induced by AC. The results suggest that AC induced toxic peripheral neuropathy might be related to disturbed β actin contents.更多还原