title: Rutaecarpine Reverses the Altered Connexin Expression Pattern Induced by Oxidized Low-density Lipoprotein in Monocytes.
abstract: Adhesion of monocytes to the vascular endothelium is crucial in atherosclerosis development. Connexins (Cxs) which form hemichannels or gap junctions, modulate monocyte-endothelium interaction. We previously found that rutaecarpine, an active ingredient of the Chinese herbal medicine Evodia, reversed the altered Cx expression induced by oxidized low-density lipoprotein (ox-LDL) in human umbilical vein endothelial cells, and consequently decreases the adhesive properties of endothelial cells to monocytes. This study further investigated the effect of rutaecarpine on Cx expression in monocytes exposed to ox-LDL. In cultured human monocytic cell line THP-1, ox-LDL rapidly reduced the level of atheroprotective Cx37 but enhanced that of atherogenic Cx43, thereby inhibiting adenosine triphosphate release through hemichannels. Pretreatment with rutaecarpine recovered the expression of Cx37 but inhibited the upregulation of Cx43 induced by ox-LDL, thereby improving adenosine triphosphate-dependent hemichannel activity and preventing monocyte adhesion. These effects of rutaecarpine were attenuated by capsazepine, an antagonist of transient receptor potential vanilloid subtype 1. The antiadhesive effects of rutaecarpine were also attenuated by hemichannel blocker 18α-GA. This study provides additional evidence that rutaecarpine can modulate Cx expression through transient receptor potential vanilloid subtype 1 activation in monocytes, which contributes to the antiadhesive properties of rutaecarpine.
authors: *Medical College, Nanchang University, Nanchang, Jiangxi Province, China; †Ganzhou Cancer Hospital, Ganzhou, Jiangxi Province, China; and ‡Jiangxi Academy of Medical Sciences, Nanchang, Jiangxi Province, China.
authors: Yong
authors: Y
authors: Liu
authors: Yan-Qi
authors: YQ
authors: Fu
authors: Wei-Jie
authors: WJ
authors: Peng
authors: Yan-Rong
authors: YR
authors: Yu
authors: Yu-Si
authors: YS
authors: Wu
authors: Hang
authors: H
authors: Yan
authors: Qi-Ren
authors: QR
authors: Huang
authors: Ming
authors: M
authors: He
authors: Dan
authors: D
authors: Luo
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D050197:Atherosclerosis / Q000503:physiopathology; D002478:Cells, Cultured; D017630:Connexins / Q000187:drug effects*; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000378:metabolism*; D006801:Humans; D026121:Indole Alkaloids / Q000494:pharmacology*; D008077:Lipoproteins, LDL / Q000378:metabolism*; D009000:Monocytes / Q000378:metabolism*; D011799:Quinazolines / Q000494:pharmacology*; D013997:Time Factors; D052999:Quinazolinones
chemical_list: D000255:Adenosine Triphosphate; D017630:Connexins; D026121:Indole Alkaloids; D008077:Lipoproteins, LDL; D011799:Quinazolines; C099252:oxidized low density lipoprotein; C028632:rutecarpine; D052999:Quinazolinones