The transcription factor-E2-related factor 2 (Nrf2) is an important regulator against the process of oxidative stress. It can effectively scavenge oxygen-free radicals within cells to maintain homeostasis. In this study, we cultured primary myocardial cells, established the hypoxia/reoxygenation (H/R) model to simulate myocardial ischemia/reperfusion injury, and examined effects of 17β-estradiol (E2) on the quantitative changes of Nrf2 in cytosolic and nuclear extracts, the mRNA expression of heme oxygenase 1 (HO-1), superoxide dismutase (Cu/Zn-SOD), glutathione S transferase (GST), and glutamate cysteine ligase amide (GCL) of each model group by Western blot assays and reverse transcription polymerase chain reaction, to investigate the effects of E2 against H/R/ injury in cultured myocardial cells. The present study shows that E2 can upregulate Nrf2 in nuclear extracts and increase the expression of HO-1, Cu/Zn-SOD, GST, and GCL significantly during H/R injury. Hence, our present findings suggest that E2 exhibits its antioxidant role by upregulating Nrf2 in nuclear extracts.
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