Key result
Bardoxolone methyl ameliorated myocardial ischemia/reperfusion injury in male rats by inhibiting oxidative stress and cardiomyocyte apoptosis via activating the Nrf2/HO-1 pathway.
Why the study?
The study was aimed at ascertaining the therapeutic efficiency and mechanism of action of bardoxolone methyl in myocardial ischemia/reperfusion injury.
Does bardoxolone methyl ameliorate myocardial ischemia/reperfusion injury in a rat model?
Does bardoxolone methyl ameliorate myocardial ischemia/reperfusion injury in a rat model?
Bardoxolone methyl protects against myocardial ischemia/reperfusion injury in rats by reducing oxidative stress and apoptosis through the Nrf2/HO-1 pathway.
Background: Myocardial ischemia/reperfusion (I/R) injury is a severe heart problem resulting from restoring coronary blood flow to the myocardium after ischemia. This study is aimed at ascertaining the therapeutic efficiency and action mechanism of bardoxolone methyl (BARD) in myocardial I/R injury. Methods: In male rats, myocardial ischemia was performed for 0.5 h, and then, reperfusion lasted for 24 h. BARD was administrated in the treatment group. The animal's cardiac function was measured. Myocardial I/R injury serum markers were detected via ELISA. The 2,3,5-triphenyltetrazolium chloride (TTC) staining was used to estimate the infarction. H&E staining was used to evaluate the cardiomyocyte damage, and Masson trichrome staining was used to observe the proliferation of collagen fiber. The apoptotic level was assessed via the caspase-3 immunochemistry and TUNEL staining. Oxidative stress was measured through malondialdehyde, 8-hydroxy-2'-deoxyguanosine, superoxide dismutase, and inducible nitric oxide synthases. The alteration of the Nrf2/HO-1 pathway was confirmed via western blot, immunochemistry, and PCR analysis. Results: The protective effect of BARD on myocardial I/R injury was observed. In detail, BARD decreased cardiac injuries, reduced cardiomyocyte apoptosis, and inhibited oxidative stress. For mechanisms, BARD treatment significantly activates the Nrf2/HO-1 pathway. Conclusion: BARD ameliorates myocardial I/R injury by inhibiting oxidative stress and cardiomyocyte apoptosis via activating the Nrf2/HO-1 pathway.
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Huang et al. (2023) studied Myocardial ischemia/reperfusion (I/R) injury. Bardoxolone methyl (BARD) was evaluated on Myocardial I/R injury (cardiac function, apoptosis, oxidative stress). Bardoxolone methyl ameliorated myocardial ischemia/reperfusion injury in male rats by inhibiting oxidative stress and cardiomyocyte apoptosis via activating the Nrf2/HO-1 pathway.
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