2. Academic Validation
  3. Galangin alleviated myocardial ischemia-reperfusion injury by enhancing autophagic flux and inhibiting inflammation

Galangin alleviated myocardial ischemia-reperfusion injury by enhancing autophagic flux and inhibiting inflammation

  • Eur J Pharmacol. 2023 Feb 25;175621. doi: 10.1016/j.ejphar.2023.175621.
Jian Zhang 1,  Shiyu Hu 2,  Yang Gao 3,  Xiang Wei 4,  Yanan Qu 3,  Rifeng Gao 4,  Yang Lv 4,  Jingpu Wang 3,  Yiwen Wang 3,  Ji'e Yang 3,  Jiatian Cao 3,  Feng Zhang 5,  Junbo Ge 6
Affiliations

Affiliations

  • 1 Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, 200032, Shanghai, China. Electronic address: [email protected].
  • 2 Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, 200032, Shanghai, China. Electronic address: [email protected].
  • 3 Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, 200032, Shanghai, China.
  • 4 Department of Cardiology, Shanghai Fifth People's Hospital, Fudan University, 200240, Shanghai, China.
  • 5 Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, 200032, Shanghai, China. Electronic address: [email protected].
  • 6 Department of Cardiology, Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, 200032, Shanghai, China; Key Laboratory of Viral Heart Diseases, National Health Commission, 200032, Shanghai, China; Key Laboratory of Viral Heart Diseases, Chinese Academy of Medical Sciences, 200032, Shanghai, China; National Clinical Research Center for Interventional Medicine, 200032, Shanghai, China; Institutes of Biomedical Sciences, Fudan University, 200032, Shanghai, China. Electronic address: [email protected].
PMID: 36849103 DOI: 10.1016/j.ejphar.2023.175621
Abstract

Autophagy is critically involved in myocardial ischemia-reperfusion (I/R). Autophagy inhibition exacerbates myocardial I/R injury. Few effective agents target Autophagy to prevent myocardial I/R injury. Effective drugs that promote Autophagy in myocardial I/R warrant further investigation. Galangin (Gal) enhances Autophagy and alleviates I/R injury. Here we conducted both in vivo and in vitro experiments to observe the changes in Autophagy after galangin treatment and investigated the cardioprotective effects of galangin on myocardial I/R.

Methods: After 45-minute occlusion of the left anterior descending coronary artery, myocardial I/R was induced by slipknot release. One day before surgery and immediately after surgery, the mice were injected intraperitoneally with the same volume of saline or Gal. The effects of Gal were evaluated using echocardiography, 2,3,5-triphenyltetrazolium chloride staining (TTC staining), western blotting, and transmission electron microscopy. Primary cardiomyocytes and bone marrow-derived macrophages were extracted in vitro to measure the cardioprotective effects of Gal.

Results: Compared with the saline-treated group, Gal significantly improved cardiac function and limited infarct enlargement after myocardial I/R. In vivo and in vitro studies demonstrated that Gal treatment promoted Autophagy during myocardial I/R. The anti-inflammatory effects of Gal were validated in bone marrow-derived macrophages. These results strongly suggest that Gal treatment can attenuate myocardial I/R injury.

Conclusion: Our data demonstrated that Gal could improve left ventricular ejection fraction and reduce infarct size after myocardial I/R by promoting Autophagy and inhibiting inflammation.

Keywords

Autophagy; Galangin; Myocardial ischemia-reperfusion.

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