Objective To explore the effect of remote ischemic postconditioning (RIPC) on calcium sensing receptorl(CaSR) expression and Akt/Pi3k pathway in brain tissue of neonatal rats with hypoxic-ischemic encephalopathy(HIE), in order to provide theoretical evidence for the treatment of HIE in neonates. Methods Totally 120 newborn Wistar rats aged 7 days were randomly divided into sham operation group (S group), hypoxic-ischemic encephalopathy group (HIE group), RIPC for 5 minutes group (R1 group) and RIPC for 10 minutes group (R2 group).The behaviors of rats in each group were observed and the body weight was measured.The morphological changes were observed by HE staining, and the ultrastructure of cells was observed by electron microscopy.The expressions of CaSR, Bax, Bcl-2,p-Akt and Akt protein were detected by immunohistochemistry, and the expression of p-Akt, Bax and Bcl-2 protein was detected by western blotting. Results Compared with HIE group, rats in R1 group and R2 group showed reduced abnormal behaviors, and the growth rate of body weight increased significantly (P<0.05).The number of CaSR positive cells in R1 group (22.00 ±1.79) and R2 group (20.83 ±2.04) was significantly lower than that in HIE group (25.67±1.21) (P < 0.05).The number of p-Akt positive cells in R1 group (25.00±1.41) and R2 group (27.3 3±1.86) was significantly more than that in HIE group (14.33 ±2.16) (P<0.05).The p-Akt optical density value of R1 group (328.33 ±24.86) and R2 group (339.67± 23.77) was significantly higher than that of HIE group (120.83 ±17.43) (P<0.05).Compared with HIE group, Bax expression level was decreased in R1 group and R2 group (P<0.05), while Bcl-2 expression level was increased (P<0.05).However, there were no significant differences on the indexes between R1 group and R2 group (P>0.05).And the Akt expression level was not significantly different among the four groups (P>0.05). Conclusion RIPC plays a protective role in neonatal rat brain tissue injury, probably because of the decreasing expression of CaSR in brain tissue and the activation of Akt/Pi3k pathway.
Key words
remote ischemia postconditioning /
hypoxic-ischemic encephalopathy /
calcium sensing receptor /
Akt/pi3k pathway
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