目的 探讨大蒜素对血管紧张素II（Ang II）诱导的心肌肥厚的保护作用及其潜在分子机制。方法 体内实验中，通过sc Ang II建立小鼠心肌肥厚模型，并给予大蒜素（10、40 mg/kg）进行干预。干预4周后，测定小鼠心脏质量指数、左心室质量指数。采用qPCR方法检测心房钠尿肽（ANP）、脑钠肽（BNP）及β-肌球蛋白重链（β-MHC）的mRNA表达水平。通过HE染色观察心脏组织形态学变化。通过Western blotting检测心脏组织中核因子（NF-κB）p65磷酸化（p-p65）及NOD样受体蛋白3（NLRP3）蛋白表达水平。体外实验中，利用Ang II诱导H9C2心肌细胞构建肥厚模型，并给予25、100 µmol/L大蒜素处理，检测心肌细胞表面积；采用qPCR法检测ANP、BNP、β-MHC mRNA表达水平；通过Western blotting和免疫荧光检测p-p65、NLRP3蛋白表达水平，并联合NF-κB激动剂佛波酯（PMA）验证该信号通路在其中的作用。结果 体内实验结果显示，大蒜素可显著降低Ang II诱导的心肌肥厚小鼠心脏质量指数、左心室质量指数（P＜0.05、0.01），减轻心肌组织病理损伤，下调心肌组织中ANP、BNP、β-MHC mRNA相对表达量（P＜0.05、0.01、0.001），并抑制p-p65、NLRP3蛋白表达（P＜0.05、0.01）。体外实验结果显示，大蒜素能显著减小Ang II诱导的心肌细胞面积（P＜0.05、0.01），下调ANP、BNP、β-MHC mRNA表达水平（P＜0.05、0.01、0.001），并抑制p-p65、NLRP3蛋白表达（P＜0.05、0.01）。经PMA处理后，大蒜素对细胞心肌肥厚的缓解作用及其对相关分子表达的抑制作用均被明显削弱。结论 大蒜素可能通过NF-κB/NLRP3信号通路减轻Ang II诱导的心肌肥厚。

Objective To investigate the protective effects of allicin on Ang II-induced cardiac hypertrophy, and its underlying molecular mechanisms. Methods In vivo experiments, the model of cardiac hypertrophy was established by subcutaneous injection of Ang II, and the mice were treated with allicin (10, 40 mg/kg). After 4 weeks of intervention, the heart weightindex and left ventricular weight index were measured. The mRNA expression levels of ANP, BNP, and β-MHC were detected by qPCR. Histomorphological changes in cardiac tissue were observed by HE staining. The protein expression levels of phosphorylated NF-κB p65 (p-p65) and NLRP3 in cardiac tissues were detected by Western blotting. In vitro experiments, H9C2 cardiomyocyte hypertrophy model was established using Ang II stimulation, followed by treatment with 25 and 100 μmol/L of allicin. The cardiomyocyte surface area was measured, and the mRNA expression levels of ANP, BNP, and β-MHC were detected by qPCR. The protein expression levels of p-p65 and NLRP3 were detected by Western blotting and immunofluorescence. The NF-κB agonist PMA was used to validate the role of this signaling pathway. Results The results of the in vivo experiments showed that allicin could significantly reduce the cardiac mass index and left ventricular mass index of mice with myocardial hypertrophy induced by Ang II (P < 0.05, 0.01), alleviate the pathological damage of myocardial tissue, down-regulate the relative expression levels of ANP, BNP, and β-MHC mRNA in myocardial tissue (P < 0.05, 0.01, 0.001), and inhibit the expression of p-p65 and NLRP3 proteins (P < 0.05, 0.01). The results of the in vitro experiments showed that allicin could significantly reduce the cell area of myocardial cells induced by Ang II (P < 0.05, 0.01), down-regulate the expression levels of ANP, BNP, and β-MHC mRNA (P < 0.05, 0.01, 0.001), and inhibit the expression of p-p65 and NLRP3 proteins (P < 0.05, 0.01). After treatment with PMA, the alleviating effect of allicin on myocardial hypertrophy and the inhibitory effect on the expression of related molecules were significantly weakened. Conclusion Allicin attenuates Ang II-induced cardiac hypertrophy, possibly through NF-κB/NLRP3 signaling pathway.

R286.2

内蒙古医学科学院公立医院科研联合基金(2025GLLH336)