RESUMEN
Objective:To explore the effect and related mechanism on inflammatory response,proliferation and apoptosis of oxLDL-induced vascular smooth muscle cell of matrine.Methods:Theatherosclerotic model was conducted through treating human aort-icvascular smooth muscle cell with oxidized low density lipoprotein(oxLDL).Cell viability and proliferation was detected by CCK-8 as-say.The mRNA level of interleukin 1 beta(IL-1β),tumor necrosis factor alpha(TNF-α),IL-10 and IL-13 was tested by quantitative real-time reverse transcription PCR(qRT-PCR).Cell apoptosis was measured by flow cytometry.The expression of proliferation marker proteins antigen identified by monoclonal antibody(Ki-67) and proliferating cell nuclear antigen(PCNA),apoptosis marker proteins B cell lymphoma 2(Bcl-2) and Bcl-2-associated X protein(Bax),signal transducer and activator of transcription 3(STAT3) and signal transducer and activator of transcription 5(STAT5) was detected by Western blot.Results: Compared with control group,the mRNA level of IL-1β and TNF-α in model group was largely increased with decreased mRNA level of IL-10 and IL-13(P<0.01).Compared with model group,the mRNA level of IL-1β and TNF-α in treatment group was attenuated with enhancive mRNA level of IL-10 and IL-13(P<0.05).Cell proliferation and apoptosis in model group was higher than control group.Cell proliferation and apoptosis in treatment group was lower than model group(P<0.05).Compared with control group,the expression of Ki-67,PCNA and Bax in model group was augmented with decreased expression of Bcl-2(P<0.01).Compared with model group,the expression of Ki-67,PCNA and Bax in treatment group declined with elevated expression of Bcl-2(P<0.05).The expression of p-STAT3 and p-STAT5 in model group was higher than control group(P<0.01).The expression of p-STAT3 and p-STAT5 in treatment group was lower than model group(P<0.05).Compared with model group,the expression of Ki-67,PCNA and Bax in treatment group and model+Ruxolitinib group was decreased with enhancive expression of Bcl-2(P<0.05).The expression of Ki-67,PCNA and Bax in model+matrine+Ruxolitinib group was observably lower than model group and the expression of Bcl-2 in model+matrine+Ruxolitinib group was observably higher than model group(P<0.01).Compared with model group,the mRNA level of IL-1β and TNF-α in treatment group,model+Ruxolitinib group and model+matrine+Ruxolitinib group was attenuated with enhancive mRNA level of IL-10 and IL-13(P<0.05).Conclusion:Matrine represses inflammation,proliferation and apoptosis of vascular smooth muscle cell by inhibiting activation of JAK/STAT3 signal pathway in atherosclerosis.