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HO-1 protects the nerves of rats with cerebral hemorrhage by regulating the PI3K/AKT signaling pathway

Authors Zhao Q, Qu R, Teng L, Yin C, Yuan Y

Received 4 December 2018

Accepted for publication 24 April 2019

Published 28 May 2019 Volume 2019:15 Pages 1459—1468

DOI https://doi.org/10.2147/NDT.S197030

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Amy Norman

Peer reviewer comments 2

Editor who approved publication: Dr Yu-Ping Ning


Qingping Zhao,1,* Rongbo Qu,2,* Lu Teng,1 Changyou Yin,1 Yuan Yuan1

1Department of Neurosurgery, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai City, Shandong Province 264000, People’s Republic of China; 2Department of Neurosurgery, Yantai Affiliated Hospital of Binzhou Medical University, Yantai City, Shandong Province 264100, People’s Republic of China

*These authors contributed equally to this work

Objective: This study aimed to investigate the neuroprotective effect of heme oxygenase-1 (HO-1) on the PI3K/AKT signaling pathway in rats with cerebral hemorrhage.
Materials and methods: Adult male Sprague-Dawley rats were randomly divided into: a sham group, a model group and an HO-1 inhibitor group (ZnPP group). Functional defects after surgery were scored according to the Longa5 standard. Hemotoxylin and eosin staining was used to detect whether the model was constructed successfully. Superoxide dismutase (SOD) vitality and malondialdehyde (MDA) content were calculated by the xanthine oxidase method and thiobarbituric acid method, respectively. Blood-brain barrier permeability was measured by Evans Blue. Apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay. The expression of Bcl-2 and BAX was evaluated by immunohistochemistry and the expression of PI3K, p-PI3K, AKT and p-AKT was tested by Western blotting.
Results: The rat intracerebral hemorrhage model was successfully constructed. Compared with the model group, the bleeding in the ZnPP group was more serious, the cell edema and deformation were aggravated, and the neurological deficit score in the rat was significantly increased. In addition, the content of Evans blue, MDA, the number of apoptotic cells, the water content of brain tissue and the expression of BAX were significantly increased, while the SOD activity and the expressions of Bcl-2, p-PI3K and p-AKT protein were decreased.
Conclusion: HO-1 could protect the nerves of rats with cerebral hemorrhage by regulating the PI3K/AKT signaling pathway.

Keywords: PI3K/AKT signaling pathway, HO-1, neuroprotection, hemorrhage

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