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Effects of hydrogen sulfide on myocardial fibrosis in diabetic rats: Changes in matrix metalloproteinases parameters

Issue title: Frontiers in Biomedical Engineering and Biotechnology – Proceedings of the 4th International Conference on Biomedical Engineering and Biotechnology, 18–21 August 2015, Shanghai, China

Guest editors: Feng Liu, Dong-Hoon Lee, Ricardo Lagoa and Sandeep Kumar

Article type: Research Article

Authors: Xiao, Ting | Zeng, Ou | Luo, Jian | Wu, Zhixiong | Li, Fang | Yang, Jun; *

Affiliations: Department of Cardiology, The First Affiliated Hospital of University of South China, Hengyang, 421001, China

Correspondence: [*] Address for correspondence: Jun Yang, Department of Cardiology, The First Affiliated Hospital of University of South China, Hengyang, 421001, China. Tel.: 0734-8578767; Fax: 0734-8279009; E-mail: [email protected].

Keywords: Hydrogen sulfide, diabetic myocardial fibrosis, matrix metalloproteinases, tissue inhibitors of metalloproteinases, transforming growth factor beta1

DOI: 10.3233/BME-151508

Journal: Bio-Medical Materials and Engineering, vol. 26, no. s1, pp. S2033-S2039, 2015

Published: 2015
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In order to explore the effects of hydrogen sulfide (H2S) on myocardial fibrosis in diabetic rats and its underlying mechanisms, intraperitoneal injections of streptozotocin were used to establish the diabetes models and sodium hydrosulfide (NaHS) was used as an exogenous donor of H2S. Eight weeks later, Van Gieson staining was used to observe pathological changes, and basic hydrolysis methods were adopted to measure hydroxyproline content, while Western Blot was used to determine the expression of MMP2, MMP7, MMP11, MMP13, MMP16, TIMP1 and TGFβ1.The results showed that significant myocardial fibrosis, decreased TIMP1 and MMP2 expression and increased MMP7, MMP11, MMP13, MMP16 expressions occurred in diabetic group, but all these changes were significantly reversed in diabetic rats after NaHS treatment. This suggests that H2S could attenuate cardiac fibrosis induced by diabetes and its mechanisms may be related to its modulation of MMPs/TIMPs expression and regulation of TGFβ1.

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