Pristimerin suppresses the phenotypic switch of vascular smooth muscle cells in atherosclerosis through inhibiting the activation of JAK2/STAT3 pathway
Affiliations 1 Department of Vascular Surgery, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, People's Republic of China. 2 Department of Electrocardiogram, Jinan Hospital, Jinan, Shandong 250000, People's Republic of China. 3 Department of Vascular Surgery, Central Hospital Affiliated to Shandong First Medical University, Jinan, Shandong 250000, People's Republic of China. 4 Department of Vascular Surgery, Nanjing Drum Tower Hospital Clinical College of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, People's Republic of China. Electronic address: qiaotongmail@nju.edu.cn.
Aim: The aim of our research was to investigate the potential effect of pristimerin on atherosclerosis , and clarify its underlying molecular mechanisms. Methods: The effect of Pris on atherosclerotic lesions were assessed by using HE staining and Oil red O staining. Moreover, serum lipid profiles also detected using the commercial reagent kits. Inflammatory factors expression was determined employing qRT-PCR. The proteins associated with the phenotypic transformation of VSMCs and JAK2/STAT3 pa...更多
Aim: The aim of our research was to investigate the potential effect of pristimerin on atherosclerosis , and clarify its underlying molecular mechanisms. Methods: The effect of Pris on atherosclerotic lesions were assessed by using HE staining and Oil red O staining. Moreover, serum lipid profiles also detected using the commercial reagent kits. Inflammatory factors expression was determined employing qRT-PCR. The proteins associated with the phenotypic transformation of VSMCs and JAK2/STAT3 pathway-related proteins were assessed using western blot, immunohistochemistry and immunofluorescence. The proliferation and migration of VSMCs were determined utilizing EdU and Transwell assay. Results: We found that Pris could suppress atherosclerotic lesions in mice. Moreover, Pris ameliorated lipid metabolism disorders and inflammation, and inhibited the phenotypic transformation of VSMCs in mice. In ox-LDL-treated VSMCs, Pris could also inhibit the phenotypic transformation and inflammatory responses. Subsequently, Pris was demonstrated to inhibit JAK2/STAT3 pathway in both HFD-caused AS mice and ox-LDL-treated VSMCs. The inhibition of Pris on the phenotypic transformation and inflammatory responses in VSMCs could be reversed by Colivelin TFA. Conclusion: Pris could alleviate the progression of AS by inhibiting the phenotypic transformation of VSMCs and inflammatory responses via suppressing the activation of JAK2/STAT3 pathway.收起
发文期刊《Pristimerin suppresses the phenotypic switch of vascular smooth muscle cells in atherosclerosis through inhibiting the activation of JAK2/STAT3 pathway》历年引证文献趋势图
