Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats

来源 :Acta Pharmacologica Sinica | 被引量 : 0次 | 上传用户:softzheng1
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Aim:To investigate the role of the endogenous cystathionine γ-synthase(CSE)/hydrogen sulfide(H_2S)pathway in vascular calcification in vivo.Methods:A ratvascular calcification model was established by administration of vitamin D3 plusnicotine(VDN).The amount of CSE and osteopontin(OPN)mRNA was deter-mined by using semi-quantitative reverse-transcription polymerase chain reaction.The calcium content,~(45)Ca~(2+) accumulation and alkaline phosphatase(ALP)activitywere measured.H,S production and CSE activity were measured.Results:yonKossa staining produced strong positive black/brown staining in areas amongthe elastic fibers of the medial layer in the calcified aorta.The calcium content,~(45)Ca~(2+) accumulation and ALP activity in calcified arteries increased by 6.77-,1.42-,and 1.87-fold,respectively,compared with controls.The expression of the OPNgene was upregulated(P<0.01).Expression of the CSE gene was downregulated.However,calcium content,~(45)Ca~(2+) uptake and ALP activity in the VDN plus NaHSgroup was lower than that in the VDN group.The content of calcium and ~(45)Ca~(2+)accumulation and activity of ALP in the aorta were 34.8%,40.75% and 63.5% lowerin the low-dosage NariS group than in the VDN group,respectively(P<0.01),andthe calcium content and deposition of ~(45)Ca~(2+) and activity of ALP was 83.9%,37.8 % and 46.2% lower in the aorta in the high-dosage NariS group than in theVDN group,respectively(P<0.01).The expression of the OPN gene wasdownregulated.Conclusion:The production of H,S,and CSE activity were de-creased and CSE gene expression was downregulated in rats with vascularcalcification.H_2S can ameliorate vascular calcification,suggesting that the H_2S/CSE pathway plays a regulatory role in the pathogenesis of vascular calcification. Aim: To investigate the role of the endogenous cystathionine γ-synthase (CSE) / hydrogen sulfide (H_2S) pathway in vascular calcification in vivo. Methods: A rat vascular calcification model was established by administration of vitamin D3 plusnicotine (VDN). CSE and osteopontin (OPN) mRNA was deter- mined by using semi-quantitative reverse-transcription polymerase chain reaction. The calcium content, ~ (45) Ca 2+ accumulation and alkaline phosphatase (ALP) activitywere measured.H, S production and CSE activity were measured. Results: yonKossa staining produced strong positive black / brown staining in areas among the elastic fibers of the medial layer in the calcified aorta. calcium content, ~ (45) Ca 2+ accumulation and ALP activity in calcified arteries increased by 6.77-, 1.42-, and 1.87-fold, respectively, compared with controls. The expression of the OPN gene was upregulated (P <0.01) .Expression of the CSE gene was downregulated.However, calcium content, ~ 45) Ca ~ (2+) uptake and ALP activity in the VDN plus NaHSgroup was lower than that in the VDN group. The content of calcium and ~ (45) Ca ~ (2+) accumulation and activity of ALP in the aorta were 34.8%, 40.75% and 63.5% lowerin the low-dosage NariS group than in the VDN group, respectively (P <0.01), and the calcium content and deposition of ~ (45) Ca ~ (2+) and activity of ALP was 83.9%, 37.8% and 46.2% lower in the aorta in the high The expression of the OPN gene was downregulated. Confluence: The production of H, S, and CSE activity were de-creased and CSE gene expression was downregulated in rats with vascularcalcification .H 2 S can ameliorate vascular calcification, suggesting that the H 2 S / CSE pathway plays a regulatory role in the pathogenesis of vascular calcification.
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