Hydrogen-rich saline reduces cerebral ischemia-reperfusion injury in rats via PI3K pathway
10.3969.j.issn.1671-7856.2017.07.003
- VernacularTitle:富氢液通过PI3K通路减轻大鼠脑缺血再灌注损伤
- Author:
Keyan CHEN
;
Wanwei DONG
- Keywords:
Hydrogen rich saline;
Ischemia reperfusion;
PI3k;
FoxO1;
Apoptosis
- From:
Chinese Journal of Comparative Medicine
2017;27(7):13-16,33
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effect of hydrogen-rich saline on apoptosis in hippocampal neurons induced by cerebral ischemia-reperfusion in rats and PI3K/Akt/FoxO1 signaling pathway.Methods The rat model of focal cerebral ischemia-reperfusion was established by thread-occlusion of the middle cerebral artery in rats.SD rats were randomly divided into sham operation group (Sham group), ischemia-reperfusion group (I/R group) and hydrogen-rich saline treatment group (HRS group), 10 rats in each group.At 24 h after reperfusion, the serum levels of IL-6, TNF-a and IL-1β were detected by ELISA.Histological changes of the hippocampus were observed by pathology using HE staining.Apoptosis in brain tissues was observed by TUNEL staining.The expression changes of p-PI3K, Akt, caspase-3 and FoxO1 proteins were detected by Western blot assay.Results Compared with the sham group, pyramidal cells were arranged loosely in the I/R group and a large number of pyramidal cells were necrotized, and the amount of apoptotic hippocampal cells was increased.The levels of IL-1β, IL-6 and TNF-α were significantly increased (P< 0.05), as well as the expression of p-PI3K, Akt and caspase-3 in the brain tissue.However, the expression of FoxO1 protein was decreased.There were significant differences between the two groups (P< 0.05).Compared with the I/R group, the inflammatory factors were significantly decreased in the HRS group.The expressions of p-PI3K, Akt and caspase-3 were also significantly decreased, while the expression of FoxO1 protein was increased (P< 0.05).Conclusions Hydrogen-rich saline can reduce brain injury caused by ischemia-reperfusion, and its mechanism may be related to PI3K/Akt/FoxO1 signaling pathway.
