2003Zhongguo bingli shengli zazhiRequires access

Inhibitory effect of hydrogen sulfide (H_2S) on cultured rat aortic smooth muscle cells

Xiaobo Chen

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Abstract

AIM: To explore the effects of hydrogen sulfide (H_2S) on proliferation of vascular smooth muscle cells (VSMC) stimulated by endothelin (ET-1, 10 -7 mol/L ) and mitrogen-activated protein kinase (MAPK) activity in VSMCs. METHODS: Cultured VSMCs were divided into six groups: (1) control group, (2) serum group, (3) endothelin group, (4) NaHS groups, (5) serum+NaHS group, and (6) endothelin+NaHS group. VSMC proliferation was measured by [ 3H]-TdR incorporation and MAPK activity in VSMC was determined by radioactivity assay. RESULTS: ET-1 increased VSMC [ 3H]-TdR incorporation by 2.39 times ( P 0.01) and MAPK activity by 1.62 times( P 0.01), as compared with control. H_2S (5×10 -5 -5×10 -4 mol/L) decreased VSMC [ 3H]-TdR incorporation and MAPK activity by 16.8%-37.4% and 7.4%-33.6%, respectively ( P 0.05 or P 0.01). CONCLUSION: This study demonstrates that H_2S inhibits ET-1-induced proliferation of VSMC,which might be mediated by the inhibition of MAPK.

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AIM: To explore the effects of hydrogen sulfide (H_2S) on proliferation of vascular smooth muscle cells (VSMC) stimulated by endothelin (ET-1, 10 -7 mol/L ) and mitrogen-activated protein kinase (MAPK) activity in VSMCs. METHODS: Cultured VSMCs were divided into six groups: (1) control group, (2) serum group, (3) endothelin group, (4) NaHS groups, (5) serum+NaHS group, and (6) endothelin+NaHS group. VSMC proliferation was measured by [ 3H]-TdR incorporation and MAPK activity in VSMC was determined by radioactivity assay. RESULTS: ET-1 increased VSMC [ 3H]-TdR incorporation by 2.39 times ( P 0.01) and MAPK activity by 1.62 times( P 0.01), as compared with control. H_2S (5×10 -5 -5×10 -4 mol/L) decreased VSMC [ 3H]-TdR incorporation and MAPK activity by 16.8%-37.4% and 7.4%-33.6%, respectively ( P 0.05 or P 0.01). CONCLUSION: This study demonstrates that H_2S inhibits ET-1-induced proliferation of VSMC,which might be mediated by the inhibition of MAPK.

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Available abstract

AIM: To explore the effects of hydrogen sulfide (H_2S) on proliferation of vascular smooth muscle cells (VSMC) stimulated by endothelin (ET-1, 10 -7 mol/L ) and mitrogen-activated protein kinase (MAPK) activity in VSMCs. METHODS: Cultured VSMCs were divided into six groups: (1) control group, (2) serum group, (3) endothelin group, (4) NaHS groups, (5) serum+NaHS group, and (6) endothelin+NaHS group. VSMC proliferation was measured by [ 3H]-TdR incorporation and MAPK activity in VSMC was determined by radioactivity assay. RESULTS: ET-1 increased VSMC [ 3H]-TdR incorporation by 2.39 times ( P 0.01) and MAPK activity by 1.62 times( P 0.01), as compared with control. H_2S (5×10 -5 -5×10 -4 mol/L) decreased VSMC [ 3H]-TdR incorporation and MAPK activity by 16.8%-37.4% and 7.4%-33.6%, respectively ( P 0.05 or P 0.01). CONCLUSION: This study demonstrates that H_2S inhibits ET-1-induced proliferation of VSMC,which might be mediated by the inhibition of MAPK.

Key concepts: Vascular smooth muscle, Endothelin 1, MAPK/ERK pathway, Endocrinology, Internal medicine, Sodium hydrosulfide, Endothelin receptor, Urotensin-II

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