Myrtenal exhibits cardioprotective effects by attenuating the pathological progression associated with myocardial infarction

Abstract

Background: Myocardial infarction poses major risks to human health because of their incredibly high rates of morbidity and mortality. Infarctions are more likely to develop as a result of dysregulation of cell death. Myrtenal can be considered for their bioactive beneficial activity in the context of cardiovascular pathologies and, particularly, in the protection toward oxidative stress followed by ischemic injury.

Objective: This study aimed to put limelight on the antioxidant, anti-apoptotic, and antibacterial properties of Myrtenal.

Methods: An in vitro model of oxidative stress-induced injury was entrenched in H9c2 cells using hydrogen peroxide, and the effects of Myrtenal were investigated. The MTT, cellular enzyme level, staining, and flow cytometry analysis were used to examine protective, antioxidant, and anti-apoptotic effects. The gene expressions were detected by qPCR. Antibacterial effect and biofilm formation were also done.

Result: The findings revealed that Myrtenal alone had negligible cytotoxic effects and that Myrtenal protects H9c2 against H₂ O₂ -induced cell death at micromolar concentrations. Myrtenal pre-treatment inhibited the generation of reactive oxygen species (ROS) as well as remarkably decreased the fluorescence intensity of ROS. Additionally, Myrtenal considerably increased the synthesis of antioxidant enzymes while dramatically decreasing the production of MDA and LDH. qPCR demonstrated the downregulation of Cas-9, TNF-α, NF-κB, P53, BAX, iNOS, and IL-6 expression while an upregulation of Bcl-2 expression in Myrtenal pre-treated groups. Myrtenal also holds the magnificent property of inhibiting bacterial growth.

Conclusion: Myrtenal ameliorates H₂ O₂ -induced cardiomyocyte injury and protects cardiomyocyte by inhibiting oxidative stress, inflammation, and apoptosis and may be a promise drug for the treatment of heart diseases.

Keywords: Myrtenal; apoptosis; cardiovascular disease; inflammation; oxidative stress.