The protective effects of distal ischemic treatment on apoptosis and mitochondrial permeability in the hippocampus after cardiopulmonary resuscitation.

Authors

Xiang Zhou, Liu Yong, Yang Huang, ShuiBo Zhu, XiaoYang Song, BiXi Li, Jian Zhu, HaiBo Wang

Published in

Journal of cellular physiology. Volume 233. Issue 9. Pages 6902-6910. Epub Mar 25, 2018.

Abstract

Apoptosis and mitochondrial dysfunction are the main cause of neurological injury after cardiopulmonary resuscitation (CPR). However, the effects of distal ischemic treatments on ischemia induced apoptosis are rarely studied, and the mechanism by which mitochondrial dysfunction contributes to CPR still unclear. A rat model of distal ischemia was established by clipping the right femoral artery. Rats were divided into blank, model, pre distal ischemic treatment, per-treatment, and post-treatment groups. Neurological deficit score was scored to evaluate neurologic function after cardiopulmonary resuscitation for 72 hr. We employed TUNEL and flow cytometry to measure the rate of apoptosis of hippocampal neurons, the integrity of mitochondrial membrane and the degree of mitochondrial permeability transition pore (mPTP) opening. The rate of apoptosis rate of hippocampal CA1 neurons in the pre-treatment and post-treatment groups were significantly lower than that of the model group. Moreover, the integrity of the mitochondrial membrane in the pre-treatment and post-treatment groups was higher than that in the model and per- treatment groups. Furthermore, the degree of mPTP opening was lower in the pre-treatment and post-treatment groups than the untreated and per-treatment groups. Taken together, our results show that ischemic preconditioning and post processing can maintain the integrity of mitochondria, perhaps by inhibiting the opening of mPTP, and reducing apoptosis of hippocampal neurons by regulating expression of apoptosis related proteins after CPR, to improve neurological function. This study highlights a novel target pathway for treatment of CPR.

PMID:
29323705
Bibliographic data and abstract were imported from PubMed on 06 Oct 2026.

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