Rutaecarpine prevented dysfunction of endothelial gap junction induced by Ox-LDL via activation of TRPV1

European Journal of Pharmacology
Wei-Jie PengDan Luo

Abstract

Gap junctions, which is formed by connexins, has been proved to play an important role in the atherogenesis development. Rutaecarpine was reported to inhibited monocyte migration, which indicates its potential for anti-atherosclerosis activity. This study evaluated the effect of rutaecarpine on endothelial dysfunction, and focused on the regulation of connexin expression in endothelial cells by rutaecarpine. Endothelia damage was induced by exposing HUVEC-12 to Ox-LDL (100mg/l) for 24h, which decreased the expression of protective proteins Cx37 and Cx40, but induced atherogenic Cx43 expression, in both mRNA and protein levels, concomitant with the impaired propidium iodide diffusion through the gap junctions. Pretreatment with rutaecarpine effectively recovered the expression of Cx37 and Cx40, but inhibited Cx43 expression, thereby improving gap junction communication and significantly prevented the endothelial dysfunction. Consequently, the cell viability and nitric oxide production were increased, lactate dehydrogenase production was decreased and monocyte adhesion was inhibited. These protective effects of rutaecarpine were remarkably attenuated by pretreatment with capsazepine, a competitive antagonist of transient receptor...Continue Reading

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Citations

Mar 16, 2018·International Journal of Molecular Sciences·Robert D Johnson, Patrizia Camelliti
Feb 28, 2018·Medicinal Research Reviews·Xiao-Fei ShangKuo-Hsiung Lee
Apr 3, 2019·Journal of Cellular Biochemistry·Arun Bahadur GurungAtanu Bhattacharjee
Jan 12, 2017·Molecular Medicine Reports·Mei Tang, Jun Fang
Dec 3, 2020·Frontiers in Cell and Developmental Biology·Jia Zheng, Chengzhi Lu

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