Department of Emergency, Wuxi Second People's Hospital Affiliated to Nanjing Medical University, 68 Zhongshan Road, Wuxi, 214002, Jiangsu, China.
Department of Cardiology, Wuxi People's Hospital Affiliated to Nanjing Medical University, 299 Qingyang Road, Wuxi, 214023, Jiangsu, China.
Cardiovasc Toxicol. 2018 Oct;18(5):393-399. doi: 10.1007/s12012-018-9449-z.
Accumulating evidence has established that systemic inflammation is an important pathophysiologic factor of coronary heart disease (CHD). In this study, we investigated whether catechin exerts anti-inflammatory function in CHD rats. CHD model of rats was established by high-fat diet feeding and pituitrin injection. The successful building of CHD model was confirmed using blood liquid biochemical analyzer. Additionally, the effects of catechin on CHD parameters and several inflammatory signaling were investigated. The levels of total cholesterol, high-density lipoprotein, low-density lipoprotein cholesterin, triglyceride and blood glucose were all significantly elevated in CHD rats compared to them in control rats, suggesting the successful establishment of CHD model. Administration of catechin attenuated CHD by reversing the levels of creatine kinase, creatine kinase-MB, lactate dehydrogenase, cardiac troponin (cTnT), ventricular ejection fraction (LVEF) and systolic internal diameter (LVIDs). Additionally, several inflammatory biomarkers or cytokines such as C-reactive protein, lipoprotein-associated phospholipase A2 (Lp-PLA2), interleukin (IL)-6 and tumor necrosis factor-alpha (TNF-α) were inhibited by catechin. In contrast to nuclear factor-kappa beta (NF-κB), several proteins involved in inflammation such as farnesoid X receptor, signal transducers and activators of transcription (STAT)-3 and protein kinase B (PKB/Akt) were all activated by catechin. Catechin could be used as a promising treatment for CHD based on its role in suppressing inflammation and balancing STAT-3 signaling.
越来越多的证据表明,系统性炎症是冠心病(CHD)的一个重要病理生理因素。在这项研究中,我们研究了儿茶素是否对 CHD 大鼠具有抗炎作用。通过高脂饮食喂养和垂体后叶素注射建立大鼠 CHD 模型。使用血液液体生化分析仪确认 CHD 模型的成功建立。此外,还研究了儿茶素对 CHD 参数和几种炎症信号通路的影响。与对照组大鼠相比,CHD 大鼠的总胆固醇、高密度脂蛋白、低密度脂蛋白胆固醇、甘油三酯和血糖水平均显著升高,表明 CHD 模型的成功建立。儿茶素的给药通过逆转肌酸激酶、肌酸激酶-MB、乳酸脱氢酶、心肌肌钙蛋白(cTnT)、心室射血分数(LVEF)和收缩期内径(LVIDs)的水平来减轻 CHD。此外,儿茶素还抑制了几种炎症生物标志物或细胞因子,如 C 反应蛋白、脂蛋白相关磷脂酶 A2(Lp-PLA2)、白细胞介素(IL)-6 和肿瘤坏死因子-α(TNF-α)。与核因子-κB 相反,儿茶素激活了几种参与炎症的蛋白质,如法尼醇 X 受体、信号转导和转录激活因子(STAT)-3 和蛋白激酶 B(PKB/Akt)。儿茶素可以作为一种有前途的 CHD 治疗方法,因为它具有抑制炎症和平衡 STAT-3 信号通路的作用。