2. Academic Validation
  3. L-theanine alleviates myocardial ischemia/reperfusion injury by suppressing oxidative stress and apoptosis through activation of the JAK2/STAT3 pathway in mice

L-theanine alleviates myocardial ischemia/reperfusion injury by suppressing oxidative stress and apoptosis through activation of the JAK2/STAT3 pathway in mice

  • Mol Med. 2024 Jun 28;30(1):98. doi: 10.1186/s10020-024-00865-0.
Qi Li # 1,  Jiaqi Ding # 1,  Boyu Xia # 1,  Kun Liu # 1,  Koulong Zheng 2,  Jingjing Wu 3,  Chao Huang 4,  Xiaomei Yuan 5,  Qingsheng You 6
Affiliations

Affiliations

  • 1 Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong University, #20 Xishi Road, Nantong, 226001, Jiangsu, China.
  • 2 Department of Cardiology, The Second Affiliated Hospital of Nantong University, Nantong, Jiangsu, China.
  • 3 Department of Cardiology, Suzhou Kowloon Hospital of Shanghai Jiaotong University School of Medicine, Suzhou, Jiangsu, China.
  • 4 Department of Pharmacology, School of Pharmacy, Nantong University, Nantong, Jiangsu, China.
  • 5 Department of Cardiology, Sichuan Provincial People's Hospital, University of Electronic Science and Technology of China, Chengdu, Sichuan, China. yuanxiaomei0903@126.com.
  • 6 Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong University, #20 Xishi Road, Nantong, 226001, Jiangsu, China. yqscy@126.com.
  • # Contributed equally.
PMID: 38943069 DOI: 10.1186/s10020-024-00865-0
Abstract

Background: L-theanine is a unique non-protein amino acid in tea that is widely used as a safe food additive. We investigated the cardioprotective effects and mechanisms of L-theanine in myocardial ischemia-reperfusion injury (MIRI).

Methods: The cardioprotective effects and mechanisms of L-theanine and the role of Janus Kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling were investigated in MIRI mice using measures of cardiac function, oxidative stress, and Apoptosis.

Results: Administration of L-theanine (10 mg/kg, once daily) suppressed the MIRI-induced increase in infarct size and serum creatine kinase and Lactate Dehydrogenase levels, as well as MIRI-induced cardiac Apoptosis, as evidenced by an increase in Bcl-2 expression and a decrease in Bax/Caspase-3 expression. Administration of L-theanine also decreased the levels of parameters reflecting oxidative stress, such as dihydroethidium, malondialdehyde, and nitric oxide, and increased the levels of parameters reflecting anti-oxidation, such as total antioxidant capacity (T-AOC), glutathione (GSH), and superoxide dismutase (SOD) in ischemic heart tissue. Further analysis showed that L-theanine administration suppressed the MIRI-induced decrease of phospho-JAK2 and phospho-STAT3 in ischemic heart tissue. Inhibition of JAK2 by AG490 (5 mg/kg, once daily) abolished the cardioprotective effect of L-theanine, suggesting that the JAK2/STAT3 signaling pathway may play an essential role in mediating the anti-I/R effect of L-theanine.

Conclusions: L-theanine administration suppresses cellular Apoptosis and oxidative stress in part via the JAK2/STAT3 signaling pathway, thereby attenuating MIRI-induced cardiac injury. L-theanine could be developed as a potential drug to alleviate cardiac damage in MIRI.

Keywords

Apoptosis; Inflammation; Ischemia/reperfusion; JAK2 /STAT3; L-theanine; Oxidative stress.

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