PMID:
Curr Mol Med. 2019 Nov 5. Epub 2019 Nov 5. PMID: 31702499
Abstract Title:
Effects of hydrogen-rich water on the PI3K/AKT signaling pathway in rats with myocardial ischemia-reperfusion injury.
Abstract:
AIMS: To confirm the effects of hydrogen-rich water on apoptosis via the PI3K/AKT signaling pathway in rats with myocardial ischemia-reperfusion injury (MIRI).BACKGROUND: 5 signaling pathways involved in the effect of hydrogen-rich water on myocardial ischemia reperfusion injury (MIRI) were analyzed.OBJECTIVE: The effects of hydrogen-rich water on apoptosis via the PI3K/AKT signaling pathway were studied in rats with myocardial ischemia-reperfusion injury (MIRI).METHOD: Sixty rats were divided randomly into a hydrogen-rich water group and control group. The hearts were removed and were fixed in a Langendorff device. The control group was perfused with K-R solution, and the hydrogen-rich water group was perfused with K-R solution + hydrogen-rich water. The two groups were then divided randomly into pre-ischemic period, ischemic period and reperfusion period groups, 10 rats per group, which were subjected to reverse perfusion for 10 min, normal treatment for 20 min, and reperfusion for 20 min, respectively. The mRNA and protein expression levels of PI3K, AKT, p-AKT, FoxO1, Bim and Caspase-3 in each group were detected by RT-qPCR, immunohistochemistry (IHC) and Western blotting.RESULT: The PI3K/AKT signaling pathway was significantly activated, while FoxO1, Bim, and Caspase-3 mRNA and protein levels were significantly decreased in the hydrogen-rich water group compared with those in the pre-ischemic and ischemic phase groups. PI3K, AKT and p-AKT mRNA and protein expression levels were increased, while the FoxO1, Bim and Caspase-3 expression levels were significantly decreased in the hydrogen-water group compared with those in the control group in the ischemia-reperfusion phase (P<0.05).CONCLUSION: Hydrogen-rich water can activate the PI3K/AKT signaling pathway, alleviate ischemia-reperfusion injury in isolated rat hearts, and inhibit cardiomyocyte apoptosis.
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