Related Experiment Video
Updated: Aug 6, 2026
Herbal Munziq Ameliorates Myocardial Ischemia-Reperfusion Injury by Inhibiting Inflammation
Published on: January 10, 2025
Allicin alleviates myocardial PANoptosis during ischemia-reperfusion by inhibiting TLR4 activation
Shichao Liang1, Jiajie Yin2, Yijie Gao3
1Department of Integrative Medicine Cardiology, China-Japan Friendship Hospital, Beijing, China; China-Japan Friendship Hospital(Institute of Clinical Medical Sciences), Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Background:
PANoptosis is a newly identified form of programmed cell death characterized by necroptosis, pyroptosis, and apoptosis. However, the mechanism of myocardial PANoptosis in myocardial ischemia-reperfusion (MI/R) remains unclear. Allicin is a promising drug for MI/R treatment, and the targets for myocardial PANoptosis remain to be explored.
Purpose:
This study aims to clarify the mechanism of myocardial PANoptosis during MI/R and therapeutic targets of allicin.
Methods:
Sprague-Dawley rats were used to establish MI/R models. Allicin (3.6 mg/kg) was injected via the tail vein 5 min before reperfusion. Myocardial damage (cardiac function, structure, cTnT, CK-MB and apoptosis), PANoptosome components (RIPK1/3, caspase-8, ASC and NLRP3), PANoptosis indicators (MLKL, GSDMD, IL-1β/18 and caspase-3) were assessed to evaluate the cardioprotective effects of allicin. Subsequently, the potential signaling pathway related to PANoptosis and therapeutic targets of allicin were screened through transcriptomic analysis, and TLR4 signaling was selected for verification. Then, H9C2 cells were used to establish an oxygen-glucose deprivation/reperfusion (OGD/R) model. The TLR4 inhibitor TAK-242, agonist RS09, and allicin were used to clarify the pathological role of TLR4 in myocardial PANoptosis and the therapeutic target of allicin by measuring the indicators of myocardial damage, PANoptosis and TLR4 expression.
Results:
In vivo experiments revealed that allicin alleviated MI/R injury and reduced both myocardial PANoptosome components and PANoptosis. Based on transcriptomic analysis and published studies, the TLR4 signaling pathway was selected to verify the pathological role in PANoptosis and the therapeutic effects of allicin. In vitro experiments demonstrated that TLR4 activation further aggravated OGD/R-induced PANoptosis and increased TLR4 expression. Conversely, both allicin and the TLR4 inhibitor suppressed myocardial PANoptosis and TLR4 expression.
Conclusion:
Allicin can reduce myocardial PANoptosis and ameliorate MI/R injury by inhibiting TLR4 activation. These findings provide a new target and strategy for the treatment of MI/R injury.
