Effects of Cytomegalovirus Infection on Coronary Artery Endothelial Cells Injury Through p38MAPK Pathway
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 30 μmol/L SB203580.Cell viability,apoptosis rate,lactate dehydrogenase(LDH),malondialdehyde(MDA),superoxide dismutase(SOD),total antioxidant capacity(T-AOC),interleukin-1β(IL-1 β),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.
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