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Effects of Hydrogen-rich Water on the PI3K/AKT Signaling Pathway in Rats with Myocardial Ischemia-reperfusion Injury

[ Vol. 20 , Issue. 5 ]

Author(s):

Liangtong Li, Xiangzi Li, Zhe Zhang, Li Liu, Tongtong Liu, Shaochun Li, Sen Liu, Yujuan Zhou* and Fulin Liu*   Pages 396 - 406 ( 11 )

Abstract:


The effects of hydrogen-rich water on PI3K/AKT-mediated apoptosis were studied in rats subjected to myocardial ischemia-reperfusion injury (MIRI).

Sixty rats were divided randomly into a hydrogen-rich water group and a control group. The hearts were removed and fixed in a Langendorff device. Hearts from the control group were perfused with K-R solution, and hearts from the hydrogen-rich water group was perfused with K-R solution + hydrogen-rich water. The two treatment 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. Caspase-3 activity was detected by spectrophotometry.

Among the hydrogen-rich water group, the PI3K/AKT signaling pathway was significantly activated, and FoxO1, Bim, and Caspase-3 mRNA and protein levels were significantly decreased in ischemia-reperfusion subgroup compared with the pre-ischemic and ischemic subgroups. In the ischemia-reperfusion hydrogen-rich water group, PI3K, AKT and p-AKT mRNA and protein expression levels were increased while the FoxO1, Bim and Caspase-3 expression levels were significantly decreased compared with those in the corresponding control group (P<0.05).

Hydrogen-rich water can activate the PI3K/AKT signaling pathway, alleviate ischemiareperfusion injury in isolated rat hearts, and inhibit cardiomyocyte apoptosis.

Keywords:

Hydrogen-rich water, myocardial ischemia-reperfusion injury, PI3K/AKT signaling pathway, FoxO1, Bim, Caspase-3, cardiomyocyte apoptosis.

Affiliation:

Medical College, Hebei University, Baoding, 071000, Medical College, Hebei University, Baoding, 071000, Medical College, Hebei University, Baoding, 071000, Medical College, Hebei University, Baoding, 071000, Affiliated Hospital of Hebei University, Baoding, 071000, Medical College, Hebei University, Baoding, 071000, Medical College, Hebei University, Baoding, 071000, Medical College, Hebei University, Baoding, 071000, Affiliated Hospital of Hebei University, Baoding, 071000



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