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Published on: January 10, 2025
Tetramethylprazine attenuates myocardial ischemia/reperfusion injury through modulation of autophagy
Zhi Zuo1, Peng-Fei Zuo1, Zu-Long Sheng1
1Department of Cardiology, Zhongda Hospital, Medical School of Southeast University, Nanjing City, JiangSu province, China.
Abstract:
The current study aimed to investigate the effects of tetramethylprazine (TMP) on myocardial ischemia/reperfusion (MI/R) injury and its underlying mechanisms. MI/R rat model and hypoxia/reoxygenation (H/R) cardiomyocytes model were established. CK level and LDH activity were detected to evaluate MI/R and H/R injury. Cell viability was determined by cell counting kit-8 (CCK-8) assay. Cell apoptosis were identified by flow cytometry and autophagy were detected by western blot. Treatment with TMP significantly reduced CK level and LDH activity and decreased myocardial infarct size in MI/R rats. TMP reduced autophagy dysfunction induced by MI/R. Moreover, TMP treatment decreased H/R-induced injury and attenuated autophagy dysfunction in cardiomyocytes. Inhibiting autophagic flux with chloroquine (CQ) decreased the cardioprotection exerted by TMP in vivo and in vitro. Additionally, the effects of TMP on the modulation of autophagy were inhibited by LY294002 (a PI3K inhibitor) in H/R cardiomyocytes. Our findings suggested TMP exerted cardioprotection against MI/R injury by decreasing Beclin-1 associated autophagy dysfunction through PI3K pathway.
Insights
Tetramethylpyrazine (TMP) protects the heart from injury caused by reduced blood flow and oxygen. It achieves this by improving autophagy dysfunction via the PI3K pathway, offering a potential therapeutic strategy for myocardial ischemia/reperfusion injury.
Area of Science:
- Cardiology
- Molecular Biology
- Pharmacology
Background:
- Myocardial ischemia/reperfusion (MI/R) injury is a significant clinical concern.
- Autophagy plays a complex role in cardiac health and disease, with dysfunction contributing to injury.
- Tetramethylpyrazine (TMP) is a compound with potential therapeutic properties.
Purpose of the Study:
- To investigate the cardioprotective effects of tetramethylpyrazine (TMP) against myocardial ischemia/reperfusion (MI/R) injury.
- To elucidate the underlying mechanisms, focusing on the role of autophagy and the PI3K pathway.
Main Methods:
- Established MI/R rat and hypoxia/reoxygenation (H/R) cardiomyocyte models.
- Assessed cardiac injury markers (CK, LDH) and infarct size.
- Evaluated cell viability (CCK-8), apoptosis (flow cytometry), and autophagy (western blot).
- Utilized chloroquine (CQ) to inhibit autophagic flux and LY294002 (PI3K inhibitor) to probe pathway involvement.
Main Results:
- TMP significantly reduced cardiac injury markers (CK, LDH) and infarct size in MI/R rats.
- TMP treatment attenuated H/R-induced injury and autophagy dysfunction in cardiomyocytes.
- Inhibition of autophagic flux with CQ diminished TMP's cardioprotective effects.
- The PI3K inhibitor LY294002 blocked TMP's modulatory effects on autophagy in H/R cardiomyocytes.
Conclusions:
- Tetramethylpyrazine (TMP) exerts significant cardioprotection against MI/R injury.
- TMP's protective effects are mediated by alleviating Beclin-1 associated autophagy dysfunction.
- The PI3K signaling pathway is crucial for TMP's mechanism of action in protecting against cardiac injury.
