Effects of combination of mild head hypothermia and IGF-1 on global cerebral ischemia-reperfusion injury in rats
Ao Li
Li Yan-li
Zhang Zhi-qiang
Bian Qing-hu
Liu Zheng
Zhang Shan
Abstract：Objective To explore the effects of combination of mild head hypothermia and IGF-1 on global cerebral ischemia-reperfusion injury in rats, and to investigate the mechanism of cerebral protection via PI3K/Akt signaling pathway. Methods Sixty healthy male SD rats weighing250 ～ 280 g were used in this study and randomly divided into five groups (n = 12): sham group (group S ), global cerebral ischemia-reperfusion injury group (group C),mild head hypothermia group (group H),IGF-1 group (group I), combination of IGF-1 and mild head hypothermia group (group HI). Modified Pulsinelli's four-vessel occlusion for 15 min was used to establish the model of global cerebral ischemia-reperfusion injury in rats. At the point of 8 h after reperfusion, six rats in each group were used to observe the immunohistochemical expression of pAkt, pFox03 a, Bcl-2 and Bax protein. The other six rats were killed to observe the expression of pAkt and total Akt protein by Western blot. Results Compared with group S,the expressions of pAkt,pFox03 a,Bcl-2 and Bax protein were all increased in group C. Compared with group C, the expression of Bax protein was reduced in group H,group I and group HI, while the expressions of pAkt, pFox03a, Bcl-2 were significantly increased. Compared with group HI, the expression of pAkt, pFox03a, Bcl-2 protein were significantly lower in group H and group I (P ＜ 0.05). Compared with group S, the expressions of pAkt protein was higher in group C. Compared with group C,the expression of pAkt protein was higher in group H, group I and group HI. The expression of pAkt protein was significantly highest in group HI (P ＜ 0.05 ). There was no statistically significant difference in the expression of total Akt protein in hippocampus with each group(P ＞ 0.05). Conclusion The combination of mild head hypothermia and IGF-1 can alleviate global ischemia-reperfusion injury, and its mechanism is likely to inhibit neuronal apoptosis via upregulating the phosphorylation of Akt and then their substrates.
Keywords：Reperfusion injuryPhosphoinositide-3-kinase/protein kinase B(PI3K/Akt)HypothermiaInsulin-like growth factor-1 (IGF-1)Cerebral protectionApoptosis
Publication Date：2018-01-01
Online Publishing Date：2025-08-15(First online date of this platform, not the publication date of the document)
Pages：5( 246-249,后插1-后插3 )