(Z)-7, 4'-dimethoxy-6-hydroxy-aurone-4-O-β-glucopyranoside attenuates lipoteichoic acid-induced damage in rat cardiomyoblast cells. Issue 8 (August 2020)

• Record Type: Journal Article
• Authors: Song, Qiang; Xie, Xuegang; Hu, Zhi; Xue, Jianying; Zhang, Songlin; Xie, Xinming
• Is Part Of: Journal of international medical research. Volume 48:Issue 8(2020)
• Publication Date: 2020-08
• Subjects: Infectious endocarditis -- (Z)-7, 4'-dimethoxy-6-hydroxy-aurone-4-O-β-glucopyranoside -- oxidative stress -- inflammatory response -- lipoteichoic acid -- apoptosis; Medicine -- Periodicals; Pharmacology -- Periodicals; 610.5
• DOI: 10.1177/0300060519889716
• Languages: English
• ISSNs: 0300-0605

Abstract

Objective: Excessive inflammatory responses in the endocardium are related to progression of infectious endocarditis. This study aimed to investigate whether (Z)-7, 4'-dimethoxy-6-hydroxy-aurone-4-O-β-glucopyranoside (DHAG), a compound isolated from the endophytic fungus Penicillium citrinum of Bruguiera gymnorrhiza, could attenuate cell damage caused by lipoteichoic acid (LTA) in embryonic rat heart cells (H9c2). Methods: LTA-induced cell damage occurred in H9c2 cells and the protective effects of DHAG at different concentrations (1–10 µM) were assessed. Indicators of oxidative stress and inflammatory responses in H9c2 cells were measured. Results: DHAG (1–10 µM) significantly attenuated LTA-induced damage in H9c2 cells, as evidenced by increased cell viability and mitochondrial membrane potential, decreased cytochrome c release and DNA fragmentation, inhibition of caspase-3 and -9 activity, and altered expression of apoptosis-related proteins. DHAG also decreased oxidative stress by increasing protein expression of nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Furthermore, DHAG inhibited inflammatory responses by decreasing protein expression of nuclear factor kappa B (NF-κB) and mitogen-activated protein kinases (MAPKs). Conclusion: DHAG exerted protective effects against LTA-induced cell damage, at least partially by decreasing oxidative stress and inhibiting inflammatory responses. Our results provide a scientific rational for developing DHAG as a therapy against infectious endocarditis.