H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins

H<sub>2</sub>S Prodrug, SG-1002, Protects against Myocardial Oxidative Damage and Hypertrophy In Vitro via Induction of Cystathionine β-Synthase and Antioxidant Proteins

Endogenously produced hydrogen sulfide (H<sub>2</sub>S) is critical for cardiovascular homeostasis. Therapeutic strategies aimed at increasing H<sub>2</sub>S levels have proven cardioprotective in models of acute myocardial infarction (MI) and heart failure (HF). The present...

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Bibliographic Details
Main Authors: Rahib K. Islam, Erinn Donnelly, Erminia Donnarumma, Fokhrul Hossain, Jason D. Gardner, Kazi N. Islam
Format: Article
Language:English
Published: MDPI AG 2023-02-01
Series:Biomedicines
Subjects:
H<sub>2</sub>S
SG-1002
oxidative stress
reactive oxygen species (ROS)
cardiovascular diseases
gasotransmitters
Online Access:https://www.mdpi.com/2227-9059/11/2/612
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Summary:Endogenously produced hydrogen sulfide (H<sub>2</sub>S) is critical for cardiovascular homeostasis. Therapeutic strategies aimed at increasing H<sub>2</sub>S levels have proven cardioprotective in models of acute myocardial infarction (MI) and heart failure (HF). The present study was undertaken to investigate the effects of a novel H<sub>2</sub>S prodrug, SG-1002, on stress induced hypertrophic signaling in murine HL-1 cardiac muscle cells. Treatment of HL-1 cells with SG-1002 under serum starvation without or with H<sub>2</sub>O<sub>2</sub> increased the levels of H<sub>2</sub>S, H<sub>2</sub>S producing enzyme, and cystathionine β-synthase (CBS), as well as antioxidant protein levels, such as super oxide dismutase1 (SOD1) and catalase, and additionally decreased oxidative stress. SG-1002 also decreased the expression of hypertrophic/HF protein markers such as atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), galectin-3, TIMP1, collagen type III, and TGF-β1 in stressed HL-1 cells. Treatment with SG-1002 caused a significant induction of cell viability and a marked reduction of cellular cytotoxicity in HL-1 cells under serum starvation incubated without or with H<sub>2</sub>O<sub>2</sub>. Experimental results of this study suggest that SG-1002 attenuates myocardial cellular oxidative damage and/or hypertrophic signaling via increasing H<sub>2</sub>S levels or H<sub>2</sub>S producing enzymes, CBS, and antioxidant proteins.
ISSN:2227-9059

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