Oxymatrine pretreatment protects H9c2 cardiomyocytes from hypoxia/reoxygenation injury by modulating the PI3K/Akt pathway

Ischemia-reperfusion (I/R) plays an important role in myocardial damage, which has been widely recognized as a key procedure in the cardiovascular disease. A hypoxia/reoxygenation (H/R) model was established using H9c2 cardiomyocytes to investigate the possible positive effect of oxymatrine (OMT), an alkaloid originating from the traditional Chinese herb Sophora flavescens Aiton, on cardiomyocytes exposed to H/R injury and the underlying molecular mechanisms. Cell viability was measured using the MTT assay, lactate dehydrogenase release measurements and hematoxylin and eosin staining. Oxidative stress was detected by measuring cellular malondialdehyde (MDA) content, as well as superoxide dismutase (SOD) and catalase (CAT) activities. Apoptosis was detected using TUNEL staining and flow cytometric analysis, and the underlying mechanism was investigated using reverse transcription-quantitative PCR and western blot analyses. The results revealed that OMT increased the viability of H9c2 cardiomyocytes exposed to H/R. The OMT pretreatment decreased the production of MDA by reactive oxygen species and increased the activities of SOD and CAT. Furthermore, the OMT pretreatment reduced the expression of Bax and caspase-3, while inducing Bcl-2 expression. In addition, the protective effect of OMT was shown to be associated with the PI3K/Akt signaling pathway, and the PI3K inhibitor LY294002 attenuated the effects of OMT on the H9c2 cardiomyocytes exposed to H/R. These findings indicate that OMT could be a potential therapeutic candidate for the treatment of myocardial ischemia/reperfusion injury.

Automated summary

OMT pretreatment showed positive effects on H9c2 cardiomyocytes exposed to H/R injury by reducing oxidative stress, decreasing apoptosis, and modulating the PI3K/Akt signaling pathway. This suggests that OMT may be a potential therapeutic candidate for myocardial ischemia/reperfusion injury.