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目的用鸡建立迟发性神经病的动物模型,观察其脑组织中蛋白激酶A(PKA)、蛋白激酶C(PKC)、β-肌动蛋白(β-actin)含量的改变。方法分为甲胺磷组、磷酸三甲苯酯组和对照组,甲胺磷组经口给予10mg/(kg·d),连续给药14d建立模型;磷酸三甲苯酯组经口给予磷酸三甲苯酯原油1ml/(kg·d),连续给药7d建立模型;对照组给予生理盐水。观察染毒组的中毒表现,染毒组和对照组母鸡于染毒后7、14、21和28d处死,利用WesternBlotting方法检测各组脑组织中PKA、PKC和β-actin含量的改变。结果甲胺磷组动物大脑中PKC与对照组比较,在染毒后的7、14、21和28d分别降低了24%(P<0.05)、28%(P<0.05)、30%(P<0.05)和62%(P<0.01),磷酸三甲苯酯组分别降低了64%(P<0.01)、58%(P<0.01)、58%(P<0.01)和43%(P<0.05)。甲胺磷组β-actin含量在14d升高了30%(P<0.05),磷酸三甲苯酯组在7d降低了26%(P<0.01)。结论在本试验条件下,甲胺磷和磷酸三甲苯酯使脑组织中的PKC含量在OPIDN的进行阶段出现降低,提示PKC含量的降低可能是OPIDN的发病机制之一。
Objective To establish an animal model of delayed neuropathy with chicken and observe the changes of protein kinase A (PKA), protein kinase C (PKC) and β-actin in brain tissues. Methods: The methamidophos group, the tricresyl phosphate group and the control group were given methamidophos. The rats in the methamidophos group were orally administered with 10 mg / (kg · d) for 14 days. The model was established by the administration of tricresyl phosphate group Ester crude oil 1ml / (kg · d), continuous administration of 7d model; control group was given saline. The toxicity of the infected group was observed. The hens of the infected and control groups were sacrificed at 7, 14, 21 and 28 d after exposure. The contents of PKA, PKC and β-actin in each group were detected by Western Blotting. Results Compared with the control group, the PKC in methamidophos group was decreased by 24% (P <0.05), 28% (P <0.05), 30% at 7, 14, 21 and 28 d after exposure (P < 58% (P <0.01), 58% (P <0.01) and 43% (P <0.05), respectively, compared with the control group (P <0.01) . The content of β-actin in methamidophos increased by 30% (P <0.05) on the 14th day and decreased by 26% on the 7th day (P <0.01). Conclusion Under the experimental conditions, methamidophos and tricresyl phosphate decreased the content of PKC in brain tissue during the progression of OPIDN, suggesting that the decrease of PKC may be one of the pathogenesis of OPIDN.