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H2S Prodrug, SG-1002, Protects Against Myocardial Oxidative Damage and Hypertrophy via Induction of Cystathionine β-Synthase and Antioxidant Proteins

Rahib K. Islam, Erinn Donnelly, Fokhrul Hossain, Jason D. Gardner, View ORCID ProfileKazi N. Islam
doi: https://doi.org/10.1101/2021.03.28.437435
Rahib K. Islam
2Departments of Pharmacology and Experimental Medicine, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA
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Erinn Donnelly
2Departments of Pharmacology and Experimental Medicine, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA
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Fokhrul Hossain
2Departments of Pharmacology and Experimental Medicine, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA
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Jason D. Gardner
3Departments of Physiology, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA
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Kazi N. Islam
1Agricultural Research Development Program, College of Engineering, Science, Technology and Agriculture, Central State University, 1400 Brush Row Road, Wilberforce, OH
2Departments of Pharmacology and Experimental Medicine, Louisiana State University Health Sciences Center, 1901 Perdido St., New Orleans, LA
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  • ORCID record for Kazi N. Islam
  • For correspondence: kislam@centralstate.edu
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Abstract

Endogenously produced hydrogen sulfide (H2S) is critical for cardiovascular homeostasis. Therapeutic strategies aimed at increasing H2S 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 H2S 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 H2O2 increased the levels of H2S, H2S 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 H2O2. Experimental results of this study suggest that SG-1002 attenuates myocardial cellular oxidative damage and/or hypertrophic signaling via increasing H2S levels or H2S producing enzyme, CBS and antioxidant proteins.

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Posted March 29, 2021.
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H2S Prodrug, SG-1002, Protects Against Myocardial Oxidative Damage and Hypertrophy via Induction of Cystathionine β-Synthase and Antioxidant Proteins
Rahib K. Islam, Erinn Donnelly, Fokhrul Hossain, Jason D. Gardner, Kazi N. Islam
bioRxiv 2021.03.28.437435; doi: https://doi.org/10.1101/2021.03.28.437435
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H2S Prodrug, SG-1002, Protects Against Myocardial Oxidative Damage and Hypertrophy via Induction of Cystathionine β-Synthase and Antioxidant Proteins
Rahib K. Islam, Erinn Donnelly, Fokhrul Hossain, Jason D. Gardner, Kazi N. Islam
bioRxiv 2021.03.28.437435; doi: https://doi.org/10.1101/2021.03.28.437435

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