The Journal of Practical Medicine ›› 2021, Vol. 37 ›› Issue (7): 858-862.doi: 10.3969/j.issn.1006⁃5725.2021.07.006

• Basic Research • Previous Articles     Next Articles

Effects of IL⁃38 on atherosclerosis in ApoE-/- mice and their mechanisms

WEI Hui,LI Hui,YU Guohua, DONG Sujuan,ZHU Weifang   

  1. The First People′s Hospital of Tianmen,Tianmen 431700,China;Hubei Province Key Laboratory of Occupational Hazard Identification and Control,Wuhan University of Science and Technology Wuhan 430065,China

  • Online:2021-04-10 Published:2021-04-10

Abstract:

Objective To explore the effects of interleukin 38(IL⁃38)on the formation of atherosclerosis and their and mechanisms in ApoE-/- mice by constructing an atherosclerosis model. Methods 6⁃week⁃old male ApoE-/- mice were randomly divided into two groups. They were fed with Western⁃style diets for 15 weeks. The mice in the control group were injected intraperitoneally with phosphate buffered solution and so were those in the model group injected with exogenous recombinant IL⁃38. After administration,the plaque areas were detected by oil red O. The plaque stability was observed;Th1,Th17,and Treg and M2 ratio in the spleen,plasma levels of IFN⁃γ IL⁃17,IL⁃10 and TGF⁃β,and serum levels of TC and TG were detected. Results As compared with the control group,the plaque areas in aortic sinus and entire aorta in the rIL⁃38 group were significantly reduced(P < 0.01 and collagen fibers and smooth muscle cells in the plaque increased significantly(P < 0.05),while CD4+ T cells macrophages,MMP⁃2,and MMP⁃9 were significantly reduced(P < 0.05);the splenic ratio of Th1 to Th17 cells in the rIL⁃38 group was significantly reduced;M2 and Treg were significantly increased;plasma levels of IFN⁃γ and IL⁃17 decreased but levels of IL⁃10 and TGF⁃βincreased(P < 0.05). Conclusions Exogenous rIL⁃38 can inhibit the process of atherosclerosis and promote the stability of plaque.

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