Article Publish Status: FREE
Abstract Title:

Melatonin attenuates AFB1-induced cardiotoxicity via the NLRP3 signalling pathway.

Abstract Source:

J Int Med Res. 2020 Oct ;48(10):300060520952656. PMID: 33081548

Abstract Author(s):

Hui Yan, Junhua Ge, Hongrui Gao, Yang Pan, Yan Hao, Jian Li

Article Affiliation:

Hui Yan


OBJECTIVE: 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.

METHODS: 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 ofand other important inflammasome components was also analysed.

RESULTS: 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.

CONCLUSION: Melatonin may reduce NLRP3 inflammasome activation by inhibiting oxidative stress and thus protect against injury from AFB1-induced myocardial toxicity.

Study Type : Animal Study

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Sayer Ji
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