Sulfur dioxide upregulates the inhibited endogenous hydrogen sulfide pathway in rats with pulmonary hypertension induced by high pulmonary blood flow

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• 作者：Liman Luo^a ; ¹ ; Die Liu^a ; ¹ ; Chaoshu Tang^b ; ^c ; Junbao Du^a ; ^c ; Angie Dong Liu^d ; Lukas Holmberg^d ; Hongfang Jin^a ; ^{jinhongfang51@126.com}
• 关键词：Pulmonary hypertension ; Pulmonary vascular remodeling ; Sulfur dioxide ; Hydrogen sulfide
• 刊名：Biochemical and Biophysical Research Communications
• 出版年：2013
• 出版时间：19 April, 2013
• 年：2013
• 卷：433
• 期：4
• 页码：519-525
• 全文大小：1870 K

文摘

Pulmonary hypertension (PH) is an important pathophysiological process in the development of many diseases. However, the mechanism responsible for the development of PH remains unknown. The objective of the study was to explore the possible impact of sulfur dioxide (SO₂) on the endogenous hydrogen sulfide (H₂S) pathway in rats with PH induced by high pulmonary blood flow. Compared with sham group, the systolic pulmonary artery pressure (SPAP) in the shunt group was significantly increased, along with the increased percentage of muscularized arteries and partially muscularized arteries of small pulmonary arteries. Compared with the shunt group, SPAP in the shunt + SO₂ group was significantly decreased, and the percentage of muscularized pulmonary arteries was also decreased. Additionally, rats that developed PH had significantly lower levels of SO₂ concentration, aspartate aminotransferase (AAT) activity, protein and mRNA expressions of AAT2 in pulmonary tissues. Administration of an SO₂ donor could alleviate the elevated pulmonary arterial pressure and decrease the muscularization of pulmonary arteries. At the same time, it increased the H₂S production, protein expression of cystathionine-¦Ã-lyase (CSE), mRNA expression of CSE, mercaptopyruvate transsulphurase (MPST) and cystathionine-¦Â-synthase (CBS) in the pulmonary tissue of the rats. The results suggested that endogenous SO₂/AAT2 pathway and the endogenous H₂S production were downregulated in rats with PH induced by high pulmonary blood flow. However, SO₂ could reduce pulmonary arterial pressure and improve the pulmonary vascular pathological changes in association with upregulating endogenous H₂S pathway.