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- W3149637578 abstract "Abstract Endogenously produced hydrogen sulfide (H 2 S) is critical for cardiovascular homeostasis. Therapeutic strategies aimed at increasing H 2 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 2 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 2 O 2 increased the levels of H 2 S, H 2 S producing enzyme, cystathionine β-synthase (CBS) as well as antioxidant protein levels, such as super oxide dismutase1 (SOD1) and catalase and decreased oxidative stress. SG-1002 also decreased the expression of hypertrophic/HF protein markers such as atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) 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 or with H 2 O 2 . Experimental results of this study suggest that SG-1002 attenuates myocardial cellular oxidative damage and/or hypertrophic signaling via increasing H 2 S levels or H 2 S producing enzyme, CBS and antioxidant proteins." @default.
- W3149637578 created "2021-04-13" @default.
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- W3149637578 date "2021-03-29" @default.
- W3149637578 modified "2023-09-26" @default.
- W3149637578 title "H2S Prodrug, SG-1002, Protects Against Myocardial Oxidative Damage and Hypertrophy via Induction of Cystathionine β-Synthase and Antioxidant Proteins" @default.
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- W3149637578 doi "https://doi.org/10.1101/2021.03.28.437435" @default.
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