丙烯酰胺对大鼠PKC、CaMKⅡ和PKA的影响  

The changes of PKC,CaMKⅡand PKA activities in spinal cord of acrylamide-intoxicated rats

作　　者：郑芸鹤[1] 黄璐[1] 齐秀清 郑秀娥[1] 张翠丽[1] 谢克勤[1] 于素芳[1] 

机构地区：[1]山东大学公共卫生学院劳动卫生与环境卫生研究所,山东济南250012 [2]临淄区卫生局卫生监督所

出　　处：《毒理学杂志》2010年第5期356-359,共4页Journal of Toxicology

基　　金：国家自然科学基金(30872088)

摘　　要：目的研究丙烯酰胺(ACR)对蛋白激酶的影响,探讨ACR中毒性神经病的发病机制。方法以20和40mg/kg ACR腹腔注射雄性Wistar大鼠8周,每周3次。利用试剂盒测定脊髓蛋白激酶C(PKC)、Ca2+-钙调蛋白依赖性蛋白激酶Ⅱ(CaMKⅡ)和蛋白激酶A(PKA)活力。结果 PKC、CaMKⅡ和PKA的活力在40 mg/kg染毒组呈明显升高的趋势,并且与对照组相比,差异有统计学意义(P<0.01)。结论在本试验条件下,脊髓PKC、CaMKⅡ和PKA的活力明显升高,提示Ca2+相关蛋白激酶活力的改变可能是ACR神经病的发病机制之一。Objective To investigate the role of the protein kinase in acrylamide（ACR） inducing toxic neuropathies.Methods ACR was administrated to male Wistar rats by intraperitoneal injection at doses of 20 or 40 mg/kg for 8 consecutive weeks（3 times per week）.The relative activities of protein kinase C（PKC）,Ca2＋-calmodulin-dependent protein kinase Ⅱ（Ca2＋/CaM-dependent kinase Ⅱ,CaMK Ⅱ） and protein kinase A（PKA） in spinal cord were determined by using SignaTECT  ProteinKinase C（PKC）,CaMKⅡand PKA activity assay kit.Results The activities of PKC,CaMKⅡ,PKA in 40 mg/kg group were significantly increased by 169.8%,260.52% and 49.7%,respectively（P 0.01）.Conclusion ACR can increase the activities of PKC,PKA and CaMKⅡwhich may be one of the toxic mechanisms of ACR-induced neuropathies.

关 键 词：丙烯酰胺 蛋白激酶 CA2+ 脊髓 

分 类 号：R135.1[医药卫生—劳动卫生]