辛伐他汀通过激活p38MAPK信号通路促进MC3T3-E1细胞增殖的研究  

Simvastatin facilitates the proliferation of MC3T3-E1 cells by activating p38MAPK signaling pathway

作　　者：韩晓梅 陈智华[1] 范希萍[1] 史冬雪 赖鑫 马茜 郑文静 HAN Xiaomei;CHEN Zhihua;FAN Xiping;SHI Dongxue;LAI Xin;MA Xi;ZHENG Wenjing(College of Veterinary Medicine,Gansu Agricultural University,Lanzhou 730070,China)

机构地区：[1]甘肃农业大学动物医学院,兰州730070

出　　处：《扬州大学学报（农业与生命科学版）》2021年第3期17-22,共6页Journal of Yangzhou University：Agricultural and Life Science Edition

基　　金：甘肃省农业生物技术项目(GNSW-2015-13)。

摘　　要：为研究辛伐他汀通过激活p38MAPK信号通路对小鼠胚胎成骨前体细胞(MC3T3-E1)增殖的影响,将试验分为2个部分:(1)将辛伐他汀作用于MC3T3-E1细胞,设置不同的辛伐他汀浓度和作用时间,采用pNPP、CCK8方法检测细胞碱性磷酸酶(ALP)活性并得到辛伐他汀对MC3T3-E1细胞增殖作用的最适浓度和最佳培养时间。(2)设3个试验组,即空白对照组、辛伐他汀组、辛伐他汀+p38抑制剂组,在辛伐他汀最适浓度和最佳培养时间的条件下,采用CCK8、pNPP、ELISA、Western blot方法检测各组细胞活力、碱性磷酸酶活性、分泌Ⅰ型胶原蛋白(COL-I)含量以及p-p38表达水平。结果表明:与空白对照组相比,当辛伐他汀浓度为10^(-5) mol·L^(-1)、培养时间为36 h时,MC3T3-E1细胞的增殖作用较为明显;空白对照组与辛伐他汀组相比,后者ALP活性和p-p38蛋白表达水平明显增高,Ⅰ型胶原蛋白分泌增多;辛伐他汀组与辛伐他汀+p38抑制剂组相比,后者ALP活性和p-p38蛋白表达水平明显降低,Ⅰ型胶原蛋白分泌减少。综合而言,辛伐他汀可通过激活p38MAPK信号通路促进MC3T3-E1的增殖,提高ALP活性和增加COL-I分泌。To study the influence of simvastatin on the proliferation of mouse embryonic osteogenic precursor cells(MC3 T3-E1)by activating the p38 MAPK signaling pathway.The experiment was divided into two parts.Part one was supplied with simvastatin with diverse concentration and duration in the cell MC3 T3-E1.pNPP and CCK8 methods were used to detect cell alkaline phosphatase(alkaline the activity of phosphatase,ALP)and viability results in the optimal concentration and optimal culture time of simvastatin to promote the proliferation of MC3 T3-E1 cells.In part two,we designed three experimental groups:blank control group,simvastatin group,simvastatin+p38 inhibitor group,under the conditions of the optimum concentration of simvastatin and the optimum incubation time,and CCK8,pNPP,enzyme-linked immuno assay adsorption technology(ELISA)and Western blot(WB)methods were used to detect cell viability,alkaline phosphatase activity,secretion of type I collagen(COL-I)and the expression level of p-p38.The results indicated that:The blank group in comparision with the proliferation effect of MC3 T3-E1 cells was more obvious when the simvastatin concentration was 10^(-5) mol·L^(-1) and the culture time was 36 h;Compared with the blank control group the simvastatin group had significantly higher ALP activity and p-p38 protein expression level,and increased type I collagen secretion;Compared with the simvastatin group,the simvastatin+p38 inhibitor group had significantly lower ALP activity and p-p38 protein expression level and reduced type I collagen secretion.In summary,simvastatin can promote the proliferation of MC3 T3-E1,increase the activity of ALP and increase the secretion of COL-I by activating the p38 MAPK signaling pathway.

关 键 词：辛伐他汀 骨质疏松 P38MAPK信号通路 

分 类 号：S859.1[农业科学—临床兽医学]