Allicin protects against LPS-induced cardiomyocyte injury by activating Nrf2-HO-1 and inhibiting NLRP3 pathways

BMC Cardiovascular Disorders

Research

Kailiang Xu¹  Guihe Duan²  Ming Lei³  Fangyuan Sun³  Jiayi Zhou³  Wei Zhang³ 

[1] Department of Critical Care Medicine, The Seventh People’s Hospital of Shanghai University of TCM, 200137, Shanghai, China;Department of Critical Care Medicine, The Shache County People’s Hospital of Xinjiang Kashgar Prefecture, 844710, Xinjiang, China;Trauma emergency center, The Seventh People’s Hospital of Shanghai University of Traditional Chinese Medicine, No.358, Datong Road, Pudong New Area, 200137, Shanghai, China;

关键词: Cardiomyocytes;    Lipopolysaccharide;    Allicin;    Apoptosis;    Inflammation;    NLR family pyrin domain containing 3;    Nuclear factor erythroid 2-related factor 2;   

DOI  :  10.1186/s12872-023-03442-1

 received in 2023-04-28, accepted in 2023-08-09,  发布年份 2023

来源: Springer

【 摘 要 】

BackgroundAllicin is a bioactive compound with potent antioxidative activity and plays a protective effect in myocardial damage and fibrosis. The role and mechanism of Allicin in septic cardiomyopathy are unclear. In this study, we investigated the effects and underlying mechanisms of Allicin on lipopolysaccharide (LPS) induced injury in H9c2 cardiomyocytes.MethodsH9c2 cardiomyocyte cells were pretreated with Allicin (0, 25, 50, and 100 µM) for 2 h, followed by incubation with LPS (10 µg/mL) for 24 h at 37 °C. Cell viability (cell counting kit-8 [CCK-8]), apoptosis (TUNEL staining), oxidative stress (malondialdehyde [MDA] and superoxide dismutase [SOD]), and cytokines release (Interleukin beta [IL-β], Interleukin 6 [IL-6], and tumor necrosis factor-alpha [TNF-α]) were determined. The mRNA and protein expression of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1), and NLR family pyrin domain containing 3 (NLRP3) signaling pathway molecules were quantified by real-time quantitative PCR (RT-qPCR) and western blot, respectively.ResultsAllicin had no effect on H9c2 cell viability but attenuated LPS-induced injury, with increased cell viability, reduction in inflammatory cytokines release, apoptosis, reduced MDA, and increased SOD (P < 0.05). Additionally, Allicin increased Nrf2 and cellular HO-1 expressions in LPS-treated H9c2 cells. Moreover, Allicin modulated the NLRP3 inflammasome, increased the cleaved caspase-1 (p10) protein, and attenuated the LPS-induced increase in NLRP3, pro-IL-1β, and IL-1β proteins. Silencing of Nrf2 by siRNA (siNrf2) significantly attenuated Allicin-induced increase in cell viability and HO-1 and decrease in NLRP3 protein in LPS-stimulated H9c2 cells.ConclusionsAllicin protects cardiomyocytes against LPS‑induced injury through activation of Nrf2/HO-1 and inhibition of NLRP3 signaling pathways.

【 授权许可】

CC BY   
© BioMed Central Ltd., part of Springer Nature 2023

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