大蒜素是一种具有强效抗氧化活性的生物活性化合物，对心肌损伤和纤维化具有保护作用。大蒜素在感染性心肌病中的作用和机制尚不清楚。本研究旨在研究大蒜素对脂多糖（LPS）诱导的H9c2心肌细胞损伤的影响及其潜在机制。将H9c2心肌细胞预处理于大蒜素（0、25、50和100µM）中2小时，然后在37°C下与LPS（10µg/mL）共培养24小时。通过细胞活力（细胞计数试剂盒-8 [CCK-8]）、细胞凋亡（TUNEL染色）、氧化应激（丙二醛 [MDA] 和超氧化物歧化酶 [SOD]）以及细胞因子释放（白细胞介素1β [IL-β]、白细胞介素6 [IL-6] 和肿瘤坏死因子α[TNF-α]）的测定，评估大蒜素的效应。用实时定量PCR（RT-qPCR）和蛋白质印迹法分别定量核因子伊瑟类红细胞相关因子2（Nrf2）、血红素氧合酶1（HO-1）和NLR家族培林结构域蛋白3（NLRP3）信号通路分子的mRNA和蛋白质表达。大蒜素不影响H9c2细胞的存活能力，但减轻了LPS诱导的损伤，提高了细胞存活能力并降低了炎症细胞因子的释放、凋亡、MDA含量，并增加了SOD的活性（P < 0.05）。此外，大蒜素提高了LPS处理的H9c2细胞中的Nrf2和细胞HO-1的表达。此外，大蒜素调节NLRP3炎症小体，增加了被剪切的caspase-1（p10）蛋白质的表达，并减轻了LPS诱导的NLRP3、前白细胞介素1β（pro-IL-1β）和白细胞介素1β（IL-1β）蛋白质的增加。通过小干扰RNA（siRNA）沉默Nrf2显著减轻了大蒜素对LPS刺激的H9c2细胞中细胞存活能力和HO-1表达的增加以及NLRP3蛋白质表达的减少。大蒜素通过激活Nrf2/HO-1信号通路并抑制NLRP3信号通路，保护心肌细胞免受LPS诱导的损伤。© 2023. BioMed Central Ltd., part of Springer Nature.

Allicin 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.H9c2 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.Allicin 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.Allicin protects cardiomyocytes against LPS‑induced injury through activation of Nrf2/HO-1 and inhibition of NLRP3 signaling pathways.© 2023. BioMed Central Ltd., part of Springer Nature.