丙烯酰胺对突触素Ⅰ上游磷酸蛋白激酶表达的影响  

STUDY ON EFFECTS OF UPSTREAM PHOSPHORIC ACID PROTEIN KINASE EXPRESSION OF SYNAPSIN I INDUCED BY ACRYLAMIDE

作　　者：王秀会[1] 张斌[1] 李忠生[1] 肖经纬[1] 李斌[1] 

机构地区：[1]中国疾病预防控制中心职业卫生与中毒控制所,北京市100050

出　　处：《中国煤炭工业医学杂志》2017年第6期692-696,共5页Chinese Journal of Coal Industry Medicine

基　　金：国家自然科学基金面上项目(编号:81273110)

摘　　要：目的探讨丙烯酰胺(acrylamide,ACR)染毒对突触素Ⅰ(SynapsinⅠ)上游丝裂原活化蛋白激酶(MAPK)、环磷酸腺苷(PKA)和Ⅱ型钙离子/钙调素依赖蛋白激酶(Ⅱ型Ca^(2+)/CaM激酶)表达的影响。方法MTT法检测不同剂量(0、25、50、75、100、125、150、200μg/ml),不同时间(24、48h)ACR染毒对成熟的NB-1细胞的毒作用;western-blot法检测突触素Ⅰ(SynapsinⅠ)的蛋白表达、SynapsinⅠ上游MAPK、PKA和Ⅱ型Ca^(2+)/CAM蛋白激酶的表达。结果 ACR对诱导成熟的NB-1具有明显的细胞毒性,细胞相对存活率随染毒剂量增加而逐渐降低,50μg/ml和100μg/ml ACR组SynapsinⅠ蛋白表达较对照组显著降低。100μg/ml ACR组MAPK蛋白表达显著降低,对照组、25和50μg/ml ACR染毒组与100μg/ml ACR组之间比较差异有统计学意义(P<0.05)。25μg/ml ACR组PKA蛋白表达显著降低,对照组、50和100μg/ml ACR染毒组与25μg/ml ACR组间差异有统计学意义(P<0.05)。25、50和100μg/ml组Ⅱ型Ca^(2+)/CaM激酶蛋白表达较对照显著增加(P<0.05),100μg/ml分别与25μg/ml与50μg/ml剂量组之间差异有统计学意义(P<0.05)。结论 ACR对诱导成熟的NB-1细胞具有明显的细胞毒性,ACR染毒可致SynapsinⅠ蛋白表达降低,且同时影响SynapsinⅠ上游的磷酸蛋白激酶MAPK、PKA和Ⅱ型Ca^(2+)/CaM的蛋白表达,可能是造成突触损伤的机制之一。Objective To explore the effects of upstream phosphoric acid protein kinase （MAPK, PKA and Ca2＋/CAM） expression of Synapsin I induced by acrylamide （ACR）.Methods Matured NB- 1 ceils were treated with gradient concentrations of ACR （0,25,50,75,100,125,150,200μg/ml） for 24 and 48h. Relative survival rate was measured by MTT method.Protein level of Synapsin I, MAPK,PKA and Ca2 ~/CAM was measured by western- blotting.Results ACR had toxic effect on matured NB- 1 ceils.Relative survival rate was increased with the concentration of ACR increased. Protein level of Synapsin I at 50μg/ml and 100 μg/ml was reduced compared with the control group after the exposure of ACR （P〈0.05）.Protein level of MAPK at 100 μg/ml ACR treatment group was decreased significantly compared with the control group and other two ACR treatment groups （25 and 50 μg/ml） （P〈0.05）.Protein level of PKA at 25 μg/ml ACR treatment group was decreased significantly compared with the control group and other two ACR treatment groups （50 and 100 μg/ml） （P 〈0.05）.Protein level of Ca2＋/CAM at ACR treatment groups （25,50 and 100 μg/ml） was increased significantly compared with the control group,and difference among ACR treatment groups were found （P〈0.05）.Conclusion ACR has toxic effect on matured NB- 1 cells.Protein level of Synapsin 1 was reduced by ACR.Protein level of upstream phosphoric acid protein kinase expression of Synapsin I is affected by ACR.Those may be one of the mechanisms of synpatic damage induced by ACR.

关 键 词：丙烯酰胺 突触素Ⅰ 丝裂原活化蛋白激酶 环磷酸腺苷 Ⅱ型钙离子/钙调素依赖蛋白激酶 

分 类 号：R744[医药卫生—神经病学与精神病学]