Cotreatments with Dex and Na2SeO3 further improved antioxidant and anti-inflammatory protection of myocardial cells from I/R injury compared to their individual treatments.

Dexmedetomidine (Dex), a sedative and analgesic agent, is known to have a cardioprotective effect against ischaemia/reperfusion (I/R) injury via regulation of antioxidant and anti-inflammatory signals. In contrast, Se shows a cardioprotective effect against I/R injury, because it is a key component of selenoproteins, most of which are antioxidant enzymes such as GPxs and TrxRs. This study aimed to determine whether the protective effects on myocardial cells against I/R injury were further improved when treatment with Dex and Se in combination. H9C2 cells were treated with Dex and Na2SeO3, alone or in combination, before oxygen glucose deprivation/reoxygenation (OGD/R). OGD/R-induced myocardial cell injury was evaluated using cell viability, apoptosis rate, the release of LDH, and intracellular ROS levels. Both Dex and Na2SeO3 improved cell viability and reduced the apoptosis rate, LDH release, and intracellular ROS. This cytoprotection was higher with Dex and Na2SeO3 cotreatment than their individual treatments. Treatment with Dex increased the SOD1, SOD2, GPx1, and GPx2 expression in H9C2 cells in OGD/R, while Na2SeO3 increased the GPx1-4 and TrxR1-3 mRNA levels. Notably, cotreatment with Dex and Na2SeO3 increased the mRNA expression of all these antioxidant enzymes. Dex treatment attenuated the activation of JNK, p65 (NF-κB), Camk1, and NLRP3 signals. Na2SeO3 enhanced the inhibitory effect of Dex on phosphorylated (p)-p65, p65, and NLRP3 in OGD/R. However, TrxR1 knockdown attenuated the positive effect of Na2SeO3 on Dex-mediated anti-inflammatory effects. In summary, cotreatments with Dex and Na2SeO3 further improved antioxidant and anti-inflammatory protection of myocardial cells from I/R injury compared to their individual treatments.