巨细胞病毒感染通过p38MAPK途径对冠状动脉内皮细胞的损伤作用  

Effects of Cytomegalovirus Infection on Coronary Artery Endothelial Cells Injury Through p38MAPK Pathway

作　　者：李玲 梁霄 杨茂 蒲盛蓝 LI Ling;LIANG Xiao;YANG Mao;PU Shenglan(The Third Affiliated Hospital of Zunyi Medical University/The First People's Hospital of Zunyi,Zunyi 563000 China)

机构地区：[1]遵义医科大学第三附属医院/遵义市第一人民医院,遵义563000

出　　处：《病毒学报》2024年第1期58-64,共7页Chinese Journal of Virology

摘　　要：巨细胞病毒(Cytomegalovirus,CMV)感染、冠状动脉内皮细胞(Human coronary artery endothelial cells,HCAEC)损伤与冠状动脉粥样硬化心脏病发生相关。CMV感染可引起细胞损伤及p38MAPK磷酸化,但对HCAEC的损伤作用及机制尚不明确。因此,为研究CMV通过p38MAPK途径对HCAEC的损伤作用,本研究培养HCAEC并分组,对照组用不含病毒及药物的培养基处理,CMV组感染HCMV AD169病毒株,SB203580组用30μmol/Lp38MAPK抑制剂SB203580处理,CMV+SB203580组感染HCMVAD169病毒株并用30μmol/L SB203580处理。检测细胞活力,凋亡率,乳酸脱氢酶(Lactate dehydrogenase,LDH)、丙二醛(Malondialdehyde,MDA)、超氧化物歧化酶(Superoxide dismutase,SOD)、总抗氧化力(Total antioxidant capacity,T-AOC)、白介素-1β(Interleukin-1β,IL-1β)、细胞间黏附分子-1(Intercellular cell adhesion molecule-1,ICAM-1)、肿瘤坏死因子-α(Tumor necrosis factor-α,TNF-α)含量,p-p38MAPK、裂解型caspase-3(cleaved caspase-3)表达水平。结果显示,与对照组比较,CMV组的细胞活力、SOD、T-AOC含量降低,凋亡率、LDH、MDA、IL-1β、ICAM-1、TNF-α含量、p-p38MAPK、cleaved caspase-3表达水平增加(P<0.05),SB203580组的p-p38MAPK表达水平降低(P<0.05),其与指标无统计学差异(P>0.05);与CMV组比较,CMV+SB203580组的细胞活力、SOD、T-AOC含量增加,凋亡率、LDH、MDA、IL-1β、ICAM-1、TNF-α含量、p-p38MAPK、cleaved caspase-3表达水平降低(P<0.05)。以上结果表明CMV感染引起HCAEC损伤及凋亡、氧化应激反应、炎症反应激活,这一作用与促进p38MAPK磷酸化有关。Cytomegalovirus(CMV)infection and human coronary artery endothelial cells(HCAEC)injury are associated with coronary atherosclerotic heart disease.CMV infection can cause cell injury and phosphorylation of p38MAPK,but the injury effect and mechanisms of CMV on HCAEC are unclear.Therefore,in order to study the injury effects of CMV on HCAECs through p38MAPK pathway,this study cultured HCAECs and divided them into groups.The control group was treated with culture medium without viruses and drugs,the CMV group was infected with HCMV AD169 virus strain,and the SB203580 group was treated with 30μmol/L p38MAPK inhibitor SB203580,the CMV+SB203580 group was infected with HCMV AD169 virus strain and treated with 30μmol/L SB203580.Cell viability,apoptosis rate,lactate dehydrogenase(LDH),malondialdehyde(MDA),superoxide dismutase(SOD),total antioxidant capacity(T‐AOC),interleukin‐1β(IL‐1β),intercellular adhesion molecule‐1(ICAM‐1),tumor necrosis factor‐α(TNF‐α)content,the expression level of p‐p38MAPK and cleaved caspase‐3 were measured.The results showed that the cell viability,SOD,T‐AOC content decreased,the apoptosis rate,LDH,MDA,IL‐1β,ICAM‐1,TNF‐αcontents,the expression level of p‐p38MAPK and cleaved caspase‐3 increased in CMV group compared with the control group(P<0.05),while the expression level of p‐p38MAPK decreased(P<0.05),other indicators had no significant difference(P>0.05)in SB203580 group.Compared with the CMV group,cell viability,SOD,T‐AOC content increased,the apoptosis rate,LDH,MDA,IL‐1β,ICAM‐1,TNF‐αcontents,the expression level of p‐p38MAPK and cleaved caspase‐3 decreased in CMV+SB203580(P<0.05).The above results suggest that CMV infection causes HCAEC injury and apoptosis,oxidative stress response,and inflammatory activation,which is related to promoting p38MAPK phosphorylation.

关 键 词：冠状动脉粥样硬化心脏病 巨细胞病毒 内皮损伤 P38MAPK 

分 类 号：R373.9[医药卫生—病原生物学]