title: Hydrogen Sulfide Improves Vascular Calcification in Rats by Inhibiting Endoplasmic Reticulum Stress.
abstract: In this study, the vitamin D3 plus nicotine (VDN) model of rats was used to prove that H2S alleviates vascular calcification (VC) and phenotype transformation of vascular smooth muscle cells (VSMC). Besides, H2S can also inhibit endoplasmic reticulum stress (ERS) of calcified aortic tissues. The effect of H2S on alleviating VC and phenotype transformation of VSMC can be blocked by TM, while PBA also alleviated VC and phenotype transformation of VSMC that was similar to the effect of H2S. These results suggest that H2S may alleviate rat aorta VC by inhibiting ERS, providing new target and perspective for prevention and treatment of VC.
authors.affiliation: Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Rui
authors.initials: R
authors.lastname: Yang
authors.affiliation: Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China; Hebei Key Lab of Laboratory Animal Science, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Xu
authors.initials: X
authors.lastname: Teng
authors.affiliation: Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Hui
authors.initials: H
authors.lastname: Li
authors.affiliation: Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Hong-Mei
authors.initials: HM
authors.lastname: Xue
authors.affiliation: Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Qi
authors.initials: Q
authors.lastname: Guo
authors.affiliation: Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
authors.forename: Lin
authors.initials: L
authors.lastname: Xiao
authors.affiliation: Department of Physiology, Institute of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China; Hebei Collaborative Innovation Center for Cardio-Cerebrovascular Disease, Shijiazhuang 050017, China; Key Laboratory of Vascular Medicine of Hebei Province, Shijiazhuang 050017, China.
authors.forename: Yu-Ming
authors.initials: YM
authors.lastname: Wu
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism* / Q000473:pathology; D002762:Cholecalciferol / Q000009:adverse effects / Q000494:pharmacology; D004195:Disease Models, Animal; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects*; D006862:Hydrogen Sulfide / Q000494:pharmacology*; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000378:metabolism* / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000378:metabolism* / Q000473:pathology; D009538:Nicotine / Q000633:toxicity; D051381:Rats; D017207:Rats, Sprague-Dawley; D061205:Vascular Calcification / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*
chemical_list: D002762:Cholecalciferol; D009538:Nicotine; D006862:Hydrogen Sulfide