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Sodium hydrosulfide alleviated pulmonary vascular structural remodeling induced by high pulmonary blood flow in rats

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Acta Pharmacologica Sinica 2006年第8期27卷 971-980页

作者： xiao-hui li~2 {3.-bao du~(2,6) ding-fang bu~3.xiu-ying tang~4.chao-{13. tang~5 ~1department of pediatrics,peking university first Hospital,key laboratory of molecular cardiovascular diseases,ministry of education ~3.laboratory Center ~4laboratory of Electron Microscopy,peking university first Hospital,Beijing 10003.,China ~5department of Physiology,peking university Health Science Center,Beijing 100083.China department of pediatrics Peking University First Hospital Key Laboratory of Molecular Cardiovascular Diseases Ministry of Education

Aim:To explore the possible role of endogenous hydrogen sulfide （H2S）,a novelgasotransmitter,in the pathogenesis of pulmonary vascular structural remodeling（PVSR） induced by high pulmonary blood ***:Thirty-two Sprague-Dawley male rats were randomly divided into sham,shunt,sham+NaHS （a H2Sdonor） and shunt+NaHS *** in shunt and shunt+NaHS groups under-went an abdominal aorta-inferior vena cava shunt,and rats in shunt+NaHS andsham+NaHS groups were intraperitoneally injected with *** was inves-tigated using optical microscope and transmission electron *** H2S was evaluated by sulfide-sensitive *** oxide synthase（NOS）,heme oxygenase （HO-1）,proliferative cell nuclear antigen （PCNA） andextracellular signal-regulated kinase （ERK） activation were analyzed by ***:After 11 weeks of shunting,PVSR developed with a decrease inlung tissue H2S production and an increase in nitric oxide （NO）.However,lungtissue carbon monoxide （CO） did not *** the treatment with NaHS for11 weeks,H2S donor ameliorated PVSR and downregulated PCNA expression andERK activation with an increase in lung tissue CO production and HO-1 proteinexpression {13.t a decrease in NO production,NOS activity and eNOS proteinexpression in shunted ***:H2S exerted a regulatory effect on PVSRinduced by high pulmonary blood ***,H2S down-regulated theERK/MAPK signal pathway,inhibited the NO/NOS pathway and enhanced theCO/HO pathway in rats with high pulmonary blood flow.

关键词： hydrogen sulfide pulmonary hypertension structure remodeling nitric oxide/nitric oxide synthase carbon monoxide/heme oxygenase

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Hydrogen sulfide induces apoptosis of pulmonary artery smooth muscle cell in rats with pulmonary hypertension induced by high pulmonary blood flow

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Chinese Medical Journal 2009年第24期122卷 3032-3038页

作者： li Wei JIN Hong-fang liU Die SUN Jing-{3. JIAN Pei-jun li xiao-{3. tang chao-shu du jun-{13. department of pediatrics Peking University First Hospital Beijing 100034 China department of pediatrics Jilin University First Hospital Changchun Jilin 130021 China department of Physiology and Pathophysiology Peking University Health Science Center Beijing 100191 China key laboratory of molecular {3. Sciences Ministry of Education Beijing 100191 China

Background Abnormal apoptosis of pulmonary artery smooth muscle cells （PASMCs） is an important pathophysiological process in the pulmonary artery structural remodeling and pulmonary hypertension. We investigated possible effect of endogenous hydrogen sulfide （H2S） on apoptosis of PASMCs during the development of pulmonary hypertension induced by high pulmonary blood flow. Methods Thirty-nine male Sprague-Dawley rats were randomly assigned to 4-week control, 4-week {3.nt, 4-week {3.nt＋propargylglycine （PPG）, 11-week control, 11-week {3.nt and 11-week {3.nt＋sodium hydrosulfide （NariS） groups. Rats in 4-week {3.nt, 4-week {3.nt＋PPG, 11-week {3.nt and 11-week {3.nt＋NariS groups underwent an abdominal aorta-inferior vena cava {3.nt. Rats in 4-week {3.nt＋PPG group were intraperitoneally injected with PPG, an inhibitor of endogenous H2S production, for 4 weeks. Rats in 11-week {3.nt＋NariS group were intraperitoneally injected with NariS, a H2S donor, for 11 weeks. Lung tissue H2S was evaluated by sulfide-sensitive electrode. Apoptosis of PASMCs were detected by terminal deoxynucleotidyl transferase mediated duTP nick end labelling （TUNEL）. Expressions of Fas, bcl-2 and caspase-3.in the PASMCs were analyzed with immunochemical staining. Results Four weeks after the {3.nting operation, the apoptosis of PASMCs and expression of Fas and caspase-3.were significantly decreased （P 〈0.01）, but expression of bcl-2 increased significantly （P 〈0.01）. PPG administration further inhibited the apoptosis of PASMCs, downregulated the expression of Fas and caspase-3.（P 〈0.01）, but increased the expression of bcl-2 （P 〈0.01）. After 11 weeks of {3.nting operation, the apoptosis of PASMCs and expression of Fas and caspase-3.were significantly decreased （P 〈0.01）, but expression of bcl-2 increased obviously （P 〈0.01）. NariS administration significantly increased the apoptosis of PASMCs, upregulated the expression of Fas and caspase-3. but inhibited the expression of bcl-2. Conclusions H2S indu

关键词： high pulmonary blood flow pulmonary hypertension hydrogen sulfide apoptosis

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Sulfur Dioxide Inhibits Extracellular Signal-regulated Kinase Signaling to Attenuate Vascular Smooth Muscle Cell Proliferation in Angiotensin II-induced Hypertensive Mice

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Chinese Medical Journal 2016年第18期129卷 2226-2232页

作者： hui-Juan Wu Ya-Qian Huang Qing-Hua Chen xiao-Yu Tian Jia liu {3.-shu tang Hong-fang Jin jun-bao du department of pediatrics Peking University First Hospital Beijing 100034 China department of Physiology and Pathophysiology Peking University Health Science Centre Beijing 100191 China key laboratory of molecular Cardiology Ministry of Education Beijing 100091 China

Background： Clarifying the mechanisms underlying vascular smooth muscle cell （VSMC） proliferation is important for the prevention and treatment of vascular remodeling and the reverse of hyperplastic lesions. Previous research has shown that the gaseous signaling molecule sulfur dioxide （SO2） inhibits VSMC proliferation, but the mechanism for the inhibition of the angiotensin Ⅱ （Angll）-induced VSMC proliferation by SO, has not been fully elucidated. This study was designed to investigate if SO2 inhibited VSMC proliferation in mice with hypertension induced by Angll. Methods： Thirty-six male C57 mice were randomly divided into control, Angll, and Angll ＋ SO2 groups. Mice in Angll group and Angl I ＋ SO2 group received a capsule-type Angll pump implanted under the skin of the back at a slow-release dose of 1000 ng-kg^-1min In addition, mice in Angll ＋ SO2 received intraperitoneal injections of SO., donor. Arterial blood pressure of tail artery was determined. The thickness of the aorta was measured by elastic fiber staining, and proliferating cell nuclear antigen （PCNA） and phosphorylated-extracellular signal-regulated kinase （P-ERK） were detected in aortic tissues. The concentration of SO~ in serum and aortic tissue homogenate supernatant was measured using high-performance liquid chromatography with fluorescence determination. In the in vio＇o study, VSMC of A7R5 cell lines was divided into six groups： control, Angll, Angll ＋ SO2 PD98059 （an inhibitor of ERK phosphorylation）, Angll ＋ PD98059, and Angll ＋ SO, ＋ PD98059. Expression of PCNA, ERK, and P-ERK was determined by Western blotting. Results： In animal experiment, compared with the control group, Angll markedly increased blood pressure （P 〈 0.01 ） and thickened the aortic wall in mice （P 〈 0.05） with an increase in the expression of PCNA （P 〈 0.05）. SO2 however, reduced the systemic hypertension and the wall thickness induced by Angli （P 〈 0.05）. It inhibited the increased expression of PCNA and P-ERK induced by A

关键词： Angiotensin II Hypertension Proliferation Sulfur Dioxide Vascular Smooth Muscle Cell

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Increased Endogenous Sulfur Dioxide Involved in the Pathogenesis of Postural Tachycardia Syndrome in Children： A Case-Control Study

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Chinese Medical Journal 2018年第4期131卷 435-439页

作者： Hong-Xia li xiao-Chun Zheng Si-Yao Chen ying liao Zhen-hui Han Pan Huang Chu-Fan Sun Jia liu Jing-Yuan Song chao-shu tang jun-bao du Yong-Hong Chen Hong-fang Jin department of pediatrics Peking University First Hospital Beijing 100034 China department of Cardiac Surgery Guangdong General Hospital Guangzhou Guangdong 510000 China department of Intensive Care Kaifeng Children's Hospital Kaifeng Henan 475000 China department of Physiology and Pathophysiology Peking University Health Science Center and Key Laboratory of Molecular Cardiology of Ministry of Education Beijing 100191 China

Background： The pathogenesis of postural tachycardia syndrome （POTS） remains unclear. This study aimed to explore the changes and significance of sulfur dioxide （SO2） in patients with POTS. Methods： The study included 3. children with POTS and 27 healthy children from peking university first Hospital between December 2013.and October 2015. A detailed medical history, physical examination results, and demographic characteristics were collected. Hemodynamics was recorded and the plasma SO2was determined. Results： The plasma SO2was significantly higher in POTS children compared to healthy children （64.0 ± 20.8 μmol/L vs. 27.2 ± 9.6 μmol/L, respectively, P 〈 0.05）. The symptom scores in POTS were positively correlated with plasma SO2levels （r = 0.3.8, P 〈 0.05）. In all the study participants, the maximum heart rate （HR） was positively correlated with plasma levels of SO2（r = 0.679, P 〈 0.01）. The change in systo{3.c blood pressure from the supine to upright （ΔSBP） in POTS group was smaller than that in the control group （P 〈 0.05）. The ΔSBP was negatively correlated with base{3.ne plasma SO2levels in all participants （r = ？0.28, P 〈 0.05）. In the control group, ΔSBP was positively correlated with the plasma levels of SO2（r = 0.487, P 〈 0.01）. The change in HR from the supine to upright in POTS was obvious compared to that of the control group. The area under curve was 0.967 （95% confidence interval： 0.928–1.000）, and the cutoff value of plasma SO2level 〉3..17 μmol/L yielded a sensitivity of 90.3. and a specificity of 92.6% for predicting the diagnosis of POTS. Conclusions： Increased endogenous SO2levels might be involved in the pathogenesis of POTS.

关键词： Blood Pressure Children: Pathogenesis Postural Tachycardia Syndrome Sulfur Dioxide

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