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选取12月龄的来亨母鸡24只,随机分为4组,分别作为赋性剂对照组和3个三邻甲苯磷酸酯(TOCP)染毒组。TCOP染毒组的动物经口一次性灌胃染毒,剂量分别为250,500,750 mg/kg,观察中毒症状,染毒后第21天处死动物,取脑组织,匀浆后Western blot测定大脑组织蛋白激酶A(PKA)、磷酸化环腺苷酸反应元件结合蛋白(CREB)、微管相关蛋白2(MAP-2)和Tau-2蛋白的含量。结果500和750mg/kg剂量组动物出现不同程度共济失调症状。低、中、高剂量组PKA含量显著升高,分别较对照组升高了23%、46%、70%(P<0.01);中、高剂量组CREB显著升高,分别较对照组升高了23%(P<0.05)、37%(P<0.01);中、高剂量组MAP2显著升高,分别较对照组升高了25%(P<0.01)、23%(P<0.05);Tau-2均未见显著性改变。
Twenty-four-month-old Leheng hens were selected and randomly divided into four groups, which were used as the control group and three tri-o-tolylphosphate (TOCP) groups. The animals in the TCOP group were given oral gavage once a day for 250, 500 and 750 mg / kg respectively. The animals were sacrificed on the 21st day after exposure and the brain tissues were harvested. After homogenization, the brain tissue protein kinase A (PKA), phosphorylated CREA, MAP-2 and Tau-2 protein. Results The animals in 500 and 750 mg / kg groups showed different degrees of ataxia symptoms. The levels of PKA in low, medium and high dose groups were significantly increased, which were respectively 23%, 46% and 70% higher than those in control group (P <0.01). The CREB levels in medium and high dose groups were significantly higher than those in control group (P <0.01). The levels of MAP2 in medium and high dose groups were significantly increased by 25% (P <0.01) and 23% (P <0.05) respectively compared with the control group. Tau-2 showed no significant change.