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Identification of a Novel Antagonist of BRS-3 from Natural Products and Its Protective Effects Against Hsub.2Osub.2-Induced Cardiomyocyte Injury
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Identification of a Novel Antagonist of BRS-3 from Natural Products and Its Protective Effects Against Hsub.2Osub.2-Induced Cardiomyocyte Injury
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Identification of a Novel Antagonist of BRS-3 from Natural Products and Its Protective Effects Against Hsub.2Osub.2-Induced Cardiomyocyte Injury
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Journal Article
Identification of a Novel Antagonist of BRS-3 from Natural Products and Its Protective Effects Against Hsub.2Osub.2-Induced Cardiomyocyte Injury
2025
Overview
The identification of exogenous ligands from natural products is an alternative strategy to explore the unrevealed physiological functions of orphan G-protein-coupled receptors (GPCRs). In this study, we have successfully identified and pharmacologically characterized licoisoflavone A (LIA) as a novel selective antagonist of BRS-3, an orphan GPCR. Functional studies showed that pretreatment with LIA ameliorated hydrogen peroxide (H[sub.2]O[sub.2])-induced cardiomyocyte injury. Furthermore, LIA pretreatment significantly restored the activities of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT), as well as lactate dehydrogenase (LDH) levels, in H9c2 cells following H[sub.2]O[sub.2] exposure. The protective effect of LIA was also evident in primary cardiomyocytes from rats and mice against H[sub.2]O[sub.2]-induced cell injury but was absent in primary cardiomyocytes derived from bombesin receptor subtype-3 knockout (Brs3 [sup.−/y]) mice, strongly confirming the mechanism of LIA’s action through BRS-3 antagonism. Proteomics studies further revealed that LIA exerted its protective effects via activating the integrin/ILK/AKT and ERK/MAPK signaling pathways. Complementary findings from Bantag-1, a well-recognized antagonist of BRS-3, in human embryonic kidney 293 mBRS-3 (HEK293-mBRS-3) stable cells and B16 cell lines, which demonstrated resistance to H[sub.2]O[sub.2]-induced damage, further supported the pivotal role of BRS-3 in oxidative stress-induced cell injury. Our study contributes to expanding our understanding of the potential pharmacological functions of BRS-3, unveiling previously unknown pharmacological functionality of this orphan receptor.
Publisher
MDPI AG
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