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目的研究苯甲基磺酰氟(PMSF)阻断有机磷诱导的迟发性神经病(OPIDN)母鸡大脑中神经丝(NFs)的动态变化和机制。方法成年母鸡随机分为正常对照组、磷酸三邻甲苯酯(tri-o-cresyl phosphate,TOCP)组和PMSF+TOCP组,Western-blotting检测母鸡染毒后第1、5、10和21天大脑中高分子量神经丝蛋白(NF-H)、中分子量神经丝蛋白(NF-M)、低分子量神经丝蛋白(NF-L)3种神经丝蛋白的相对含量。结果TOCP染毒后母鸡出现OPIDN症状,大脑中NFs含量明显改变,且大脑沉淀中比上清中变化更加明显。总的趋势是从第1天开始降低,第10天达到最低,第21天有所恢复。大脑沉淀中NF-L、NF-M和NF-H在第10天分别降低了86.22%(P<0.01),86.98%(P<0.01),54.05%(P<0.05)。提前24 h给予PMSF后,与正常对照相比,母鸡未出现明显OPIDN症状,大脑上清和沉淀中NF-L和NF-M均无明显变化,NF-H有所增加,在沉淀中第5天增加最多达109.05%(P<0.01)。沉淀中PMSF+TOCP组NF 3个亚单位比TOCP组在各时间点均有不同程度的增加。结论TOCP染毒引起母鸡大脑中NFs紊乱,提前给予PMSF能够抑制这种变化,提示TOCP诱发的NF紊乱可能是OPIDN发生的一种机制。
Objective To investigate the dynamic changes and mechanisms of PMSF in blocking the neurofilament (NFs) in the brain of OPIDN hen induced by organophosphorus. Methods Adult hens were randomly divided into normal control group, tri-o-cresyl phosphate (TOCP) group and PMSF + TOCP group. Western hematoxylin and eosin The content of high molecular weight neurofilament protein (NF-H), middle molecular weight neurofilament protein (NF-M) and low-molecular-weight neurofilament protein (NF- Results The hemorrhagic symptoms of OPIDN were observed in the hens after TOCP exposure. The contents of NFs in the brain were significantly changed and the changes in the brain sediments were more obvious than those in the supernatant. The general trend is to decrease from day 1, to reach the lowest on day 10 and to recovery on day 21. The brain deposition of NF-L, NF-M and NF-H decreased by 86.22% (P <0.01), 86.98% (P <0.01) and 54.05% (P <0.05) on the 10th day. Compared with the control group, there was no obvious OPIDN symptom in the hens at 24 h after PMSF administration. There was no significant change in NF-L and NF-M in the supernatant and sediment in the supernatant, while NF-H was increased. Day increase up to 109.05% (P <0.01). Precipitation in the PMSF + TOCP NF 3 subunits than the TOCP group at different time points increased in varying degrees. Conclusion TOCP exposure can cause NFs disorder in the hen brain. Pretreatment with PMSF can inhibit this change, suggesting that TOCP-induced NF disorder may be a mechanism of OPIDN.