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Exogenous H2S mitigates myocardial fibrosis in diabetic rats through suppression of the canonical Wnt pathway.

Abstract：

:Hydrogen sulfide (H2S) has antifibrotic activity in the kidneys, heart, lungs, and other organs. The present study investigated the protective activity of exogenous H2S against myocardial fibrosis in a rat model of diabetes. Animals were assigned to normal control, diabetes mellitus (DM), DM + sodium hydrosulfide (NaHS; DM + NaHS) and NaHS groups. Fasting blood glucose (FBG), cardiac function and hydroxyproline were monitored. Heart histomorphology and ultrastructure were additionally evaluated. Wnt1‑inducible signaling pathway protein (WISP)‑1 protein expression in the myocardium was determined by immunohistochemical staining. Matrix metalloprotease (MMP)‑2, tissue inhibitor of metalloproteinase (TIMP)‑2, collagens, and canonical Wnt and transforming growth factor (TGF)‑β1/SMAD family member 3 (Smad3) pathway‑related proteins were assessed by western blotting. Cardiac function was decreased, and myocardial injury, hypertrophy and fibrosis were increased in the diabetes model rats. MMP‑2 expression was decreased, and the expressions of WISP‑1, TIMP‑2, collagens, and canonical Wnt and TGF‑β1/Smad3 pathway‑related proteins were increased in the myocardia of the diabetes model rats. The present results indicated that the canonical Wnt pathway promoted diabetic myocardial fibrosis by upregulating the TGF‑β1/Smad3 pathway. Except for FBG, exogenous H2S ameliorated the changes in diabetes‑associated indices in rats in the DM + NaHS group. The results are consistent with H2S protection of streptozotocin‑induced myocardial fibrosis in the diabetes model rats by downregulation of the canonical Wnt and TGF‑β1/Smad3 pathway and decreased myocardial collagen deposition.

journal_name

Int J Mol Med

journal_title

International journal of molecular medicine

authors

Yang R,Jia Q,Ma SF,Wang Y,Mehmood S,Chen Y

doi

10.3892/ijmm.2019.4237

subject

Has Abstract

pub_date

2019-08-01 00:00:00

pages

549-558

issue

2

eissn

1107-3756

issn

1791-244X

journal_volume

44

pub_type

杂志文章

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