Effects of penehyclidine hydrochloride on myocardial ischaemia-reperfusion injury in rats by inhibiting TLR4/MyD88/NF-κB pathway via miR-199a-3p

被引:1
作者
Bai, Ling Qiang [1 ]
Wang, Bin Zhe [2 ]
Liu, Qi Wei [1 ]
Li, Wen Qiang [1 ]
Zhou, Hang [1 ]
Yang, Xiao Yan [1 ]
机构
[1] Baoji High Tech Hosp, Dept Cardiovasc Med, 19 Hexie Rd, Baoji 721006, Shaanxi, Peoples R China
[2] 940th Hosp Joint Logist Support Force Chinese Peo, Dept Outpatients 1, Lanzhou, Peoples R China
关键词
Penehyclidine; myocardial ischaemia-reperfusion; miR-199a-3p; improving; ISCHEMIA/REPERFUSION INJURY; MITOCHONDRIAL DYNAMICS; KAPPA-B; CARDIOPROTECTION; CARDIOMYOCYTES; PROTECTION;
D O I
10.1080/08977194.2022.2109469
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
This study was to probe the role of penehyclidine hydrochloride (PHC) mediating the impact of toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor-kappa B (NF-KB) signalling pathway on myocardial ischaemia-reperfusion injury (MI/RI) in rats through miR-199a-3p. The rat MI/RI model was established through ligating left anterior descending (LAD) coronary artery. PHC was injected preoperatively into the model rats, and injected with miR-199a-3p lentiviral vector or TLR4 antagonist (TAK-242). Next, cardiac function of rats was examined by echocardiography, and rat serum indicators, oxidative stress levels and inflammatory factors were detected. HE staining was applied to detect pathological tissue structure, TUNEL staining to detect apoptosis rate, qRCR and western blot to detect miR-199a-3p and TLR4/MyD88/NF-kappa B expressions in rat myocardial tissues. Dual luciferase reporter experiment was conducted to confirm the relationship between miR-199a-3p and TLR4. In conclusion, PHC suppresses TLR4/MyD88/NF-kappa B signalling pathway through miR-199a-3p, thereby improving MI/RI in rats. [GRAPHICS]
引用
收藏
页码:186 / 199
页数:14
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