目的 基于AMP活化蛋白激酶（AMPK）/雷帕霉素哺乳靶蛋白（mTOR）/核转录因子-κB（NF-κB）信号通路探究槲皮素对川崎病大鼠冠状动脉炎症及心肌损伤的影响。方法 将幼鼠随机分为对照组、模型组、槲皮素（14、28、56 mg/kg）组、槲皮素＋Compound C组。检测幼鼠心功能、血清心肌损伤和炎性相关因子水平；观察幼鼠心肌组织病理损伤和细胞凋亡变化；检测幼鼠心肌组织凋亡以及AMPK/mTOR/NF-κB信号通路相关蛋白表达。结果 与模型组比较，槲皮素组幼鼠心肌组织冠状动脉内膜损伤以及炎性细胞浸润和线粒体结构损伤减轻，左室射血分数（LVEF）、左室缩短分数（LVFS）、B细胞淋巴瘤-2基因（Bcl-2）、p-AMPK/AMPK蛋白表达显著增加，肌酸激酶同工酶（CK-MB）、肌酸激酶（CK）、乳酸脱氢酶（LDH）、白细胞介素（IL）-6、IL-8、IL-18、心肌细胞凋亡率、Bcl-2相关X蛋白（Bax）、活化型半胱氨酸天冬氨酸蛋白酶-3（cleaved Caspase-3）、p-mTOR/mTOR、p-NF-κB p65/NF-κB p65蛋白表达显著下降（P＜0.05）；与槲皮素56 mg/kg组比较，槲皮素＋Compound C组幼鼠心肌组织冠状动脉内膜损伤和线粒体结构损伤加重，心肌细胞出现核固缩，炎性细胞浸润增加，LVEF、LVFS、Bcl-2、p-AMPK/AMPK蛋白表达显著下降，CK-MB、CK、LDH、IL-6、IL-8、IL-18、心肌细胞凋亡率、Bax、cleaved Caspase-3、p-mTOR/mTOR、p-NF-κB p65/NF-κB p65蛋白表达显著增加（P＜0.05）。结论 槲皮素通过调控AMPK/mTOR/NF-κB信号通路，减轻川崎病大鼠冠状动脉炎症，改善心肌损伤。

Objective To explore the effects of quercetin on coronary artery inflammation and myocardial damage in Kawasaki disease rats based on the AMPK/mTOR/NF-κB signaling pathway. Methods Mice were randomly divided into control group, model group, quercetin (14, 28, 56 mg/kg) groups, and the quercetin + Compound C group. The cardiac function, serum levels of myocardial injury and inflammatory-related factors of mice were detected, the pathological damage of myocardial tissue and the changes of cell apoptosis in the mice were observed, the apoptosis of myocardial tissue and the expression of related proteins in the AMPK/mTOR/NF-κB signaling pathway were detected. Results Compared with model group, the coronary artery intimal injury, inflammatory cell infiltration and mitochondrial structure damage in the myocardial tissue of mice in the quercetin group were alleviated, while the LVEF, LVFS, Bcl-2, and p-AMPK/AMPK protein expression were significantly increased. CK-MB, CK, LDH, IL-6, IL-8, IL-18, myocardial cell apoptosis rate, Bax, cleaved Caspase-3, p-mTOR/mTOR, and p-NF-κB p65/NF-κB p65 protein expression were significantly decreased (P < 0.05). Compared with quercetin 56 mg/kg group, the myocardial tissue of mice in the quercetin + Compound C group showed aggravated coronary artery intimal injury and mitochondrial structure damage, with nuclear pyknosis in myocardial cells, increased inflammatory cell infiltration, and significant decreases in LVEF, LVFS, Bcl-2, and p-AMPK/AMPK protein expression. CK-MB, CK, LDH, IL-6, IL-8, IL-18, myocardial cell apoptosis rate, Bax, cleaved Caspase-3, p-mTOR/mTOR, and p-NF-κB p65/NF-κB p65 protein expression were significantly increased (P< 0.05). Conclusion Quercetin reduces coronary artery inflammation and improves myocardial damage in Kawasaki disease rats by regulating the AMPK/mTOR/NF-κB signaling pathway.

R285.5

河南省医学科技攻关计划联合共建项目（LH-GJ20210752）