Yan Hui, Ge Junhua, Gao Hongrui, Pan Yang, Hao Yan, Li Jian
Department of Cardiology, College of Medical Sciences, Qingdao University, Shandong, China.
Department of Cardiology, The Affiliated Hospital of Qingdao University, Shandong, China.
J Int Med Res. 2020 Oct;48(10):300060520952656. doi: 10.1177/0300060520952656.
This study was conducted to investigate the protective effect of melatonin against aflatoxin B1 (AFB1) cardiotoxicity by evaluating NOD-like receptor family pyrin domain containing protein 3 (NLRP3) signalling.
Four groups of five rats each were assessed: control group (vehicle only), two AFB1 (0.15 and 0.3 mg/kg)-treated groups, and a combined AFB1 (0.3 mg/kg) plus melatonin (5 mg/kg)-treated group. After 6 weeks of once-daily intragastric treatment, cardiac pathologic changes were observed under optical microscopy, and oxidative/antioxidative parameters were measured in myocardial homogenate. Cardiac tissue expression of and other important inflammasome components was also analysed.
Compared with controls, increasing concentrations of AFB1 were associated with increased oxidative stress and caused myocardial structure damage. In addition, AFB1 dose-dependently activated the NLRP3 signalling pathway. All these indices were significantly ameliorated by combined AFB1 plus melatonin treatment versus high-dose AFB1 alone.
Melatonin may reduce NLRP3 inflammasome activation by inhibiting oxidative stress and thus protect against injury from AFB1-induced myocardial toxicity.
本研究旨在通过评估含NOD样受体家族吡咯结构域蛋白3（NLRP3）信号通路，探讨褪黑素对黄曲霉毒素B1（AFB1）心脏毒性的保护作用。
将20只大鼠分为四组，每组5只：对照组（仅给予溶剂）、两个AFB1处理组（0.15和0.3mg/kg）以及一个AFB1（0.3mg/kg）加褪黑素（5mg/kg）联合处理组。每日一次灌胃治疗6周后，在光学显微镜下观察心脏病理变化，并测定心肌匀浆中的氧化/抗氧化参数。同时分析心脏组织中NLRP3及其他重要炎性小体成分的表达。
与对照组相比，AFB1浓度升高与氧化应激增加相关，并导致心肌结构损伤。此外，AFB1剂量依赖性激活NLRP3信号通路。与单独高剂量AFB1处理相比，AFB1加褪黑素联合处理显著改善了所有这些指标。
褪黑素可能通过抑制氧化应激来降低NLRP3炎性小体的激活，从而预防AFB1诱导的心肌毒性损伤。
