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Atherosclerosis is a common disease. It is a serious hazard to human health,which mainly involved in large arteries and affect a number of important organs. Research has shown that the proliferation, apoptosis and intimal migration of vascular smooth muscle cells (VSMC) are the key factors to the development of atherosclerosis and its complications. Recent studies show that atherosclerosis is a essentially chronic immune inflammatory disease. The inflammatory factors in atherosclerosis and its complications play important roles in the development process, thus the role of inflammatory factors on VSMC proliferation, migration, secretion and apoptosis will naturally become a concern subject to the domestic and foreign scholars.IL-32 (interleukin 32, IL-32) is a newly discovered proinflammatory cytokine. Over several years study I found that IL-32 can promote cell differentiation, apoptosis, induce other proinflammatory cytokines and chemokines by multiple signal transduction pathways, and play an important role in inflammation and autoimmune diseases. IL-32 is an important proinflammatory cytokine and an inducer of proinflammatory cytokines and chemokines, and play an important role in rheumatoid arthritis, but also has the characteristics of accelerated atherosclerosis, I propose that IL-32 may play a regulatory role on VSMC proliferation, migration, apoptosis and secretion, and may be an important new target for preventing atherosclerosis.The Wistar rat vascular smooth muscle cells were used in my study,I examined the effects of different concentrations of IL-32γ(10,50,100 ng/ml) on the Proliferation capability of VSMC by MTT. I detect the effect on the cycle and apoptosis of VSMC after adding IL-32γand NF-кB and the MAPKs pathway inhibitors (PDTC is the NF-κB inhibitor, PD98059 is ERK1/2 specific inhibitor, SB203580 is a specific inhibitor of p38MAPK, SP600125 is a specific inhibitor of JNK) by flow cytometry. RT-PCR detects mRNA expression of. IGF-1, IGFBP-3, MMP-2, TIMP-1.In conclusion, I found that IL-32γcan promote cell proliferation, migration and inhibit apoptosis. Therefore, IL-32γmay play a role in accelerating the development of atherosclerosis.
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