Medicinal and Biomolecular Chemistry Laboratory, Department of Biochemistry and Biotechnology, Annamalai University, Annamalai Nagar, 608 002, Tamil Nadu, India.
Eur J Pharmacol. 2022 Jun 5;924:174909. doi: 10.1016/j.ejphar.2022.174909. Epub 2022 Mar 25.
Myocardial infarction (MI) is a life-threatening condition. No studies were conducted earlier on the effects of (-) epicatechin (EC) on tachycardia, cardiac hypertrophy, and inflammation in MI. Hence, the preventive effects of EC on tachycardia, cardiac hypertrophy, and nuclear factor- κB inflammatory signaling pathway in experimental MI were appraised. This investigation included 4 groups of 24 male albino Wistar rats. Group:1. Normal control, Group: 2. EC (20 mg/kg body weight), Group: 3. Isoproterenol (100 mg/kg body weight), Group:4. EC (20 mg/kg body weight) + Isoproterenol (100 mg/kg body weight). MI was created in rats by isoproterenol (100 mg/kg body weight). The heart rate, heart weight, plasma myoglobin, serum cardiac troponin I, heart conjugated dienes, serum high-sensitivity C-reactive protein, and plasma total homocysteine were considerably (P < 0.05) raised in isoproterenol-induced myocardial infarcted rats. Further, reverse transcription-polymerase chain reaction study revealed a considerable (P < 0.05) increase in the expressions of heart pro-inflammatory cytokines such as nuclear factor- κB, tumor necrosis factor-α, interleukin-1β, interleukin-6, and a considerable (P < 0.05) decrease in anti-inflammatory cytokine gene, interleukin-10 in myocardial infarcted rats. Non-enzymatic antioxidants such as vitamin C, and vitamin E were considerably (P < 0.05) lessened in the heart. EC (20 mg/kg body weight) pre-treatment orally, daily, for 3 weeks prevented all changes in the above-mentioned functional, structural, biochemical, and molecular parameters investigated and improved cardiac function. The possible mechanisms are EC's anti-tachycardial, anti-cardiac hypertrophic, antioxidant, and anti-inflammatory effects.
心肌梗死（MI）是一种危及生命的疾病。以前没有研究过 (-)表儿茶素（EC）对 MI 中的心动过速、心脏肥大和炎症的影响。因此，评估了 EC 对实验性 MI 中心动过速、心脏肥大和核因子-κB 炎症信号通路的预防作用。这项研究包括 4 组 24 只雄性白化 Wistar 大鼠。组 1. 正常对照组，组 2. EC（20mg/kg 体重），组 3. 异丙肾上腺素（100mg/kg 体重），组 4. EC（20mg/kg 体重）+异丙肾上腺素（100mg/kg 体重）。异丙肾上腺素（100mg/kg 体重）诱导大鼠发生 MI。异丙肾上腺素诱导的心肌梗死大鼠的心率、心脏重量、血浆肌红蛋白、血清心肌肌钙蛋白 I、心脏共轭二烯、血清高敏 C 反应蛋白和血浆总同型半胱氨酸显着升高（P<0.05）。此外，逆转录-聚合酶链反应研究表明，心脏促炎细胞因子如核因子-κB、肿瘤坏死因子-α、白细胞介素-1β、白细胞介素-6 的表达显着增加（P<0.05），抗炎细胞因子基因，白细胞介素-10 在心肌梗死大鼠中显着减少（P<0.05）。非酶抗氧化剂，如维生素 C 和维生素 E，在心脏中显着减少（P<0.05）。EC（20mg/kg 体重）口服，每日一次，连续 3 周预处理可预防上述所有功能、结构、生化和分子参数的变化，并改善心脏功能。可能的机制是 EC 的抗心动过速、抗心脏肥大、抗氧化和抗炎作用。
