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Neuroprotective effects of curdione against focal cerebral ischemia reperfusion injury in rats

Authors Li XJ, Liang L, Shi HX, Sun XP, Wang J, Zhang LS

Received 11 April 2017

Accepted for publication 7 June 2017

Published 30 June 2017 Volume 2017:13 Pages 1733—1740

DOI https://doi.org/10.2147/NDT.S139362

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Prof. Dr. Roumen Kirov

Peer reviewer comments 2

Editor who approved publication: Professor Wai Kwong Tang


Xing-Jie Li,1,* Li Liang,2,* Hong-Xia Shi,1 Xiao-Ping Sun,1 Jing Wang,1 Lian-Sheng Zhang1

1Health Management Center, Lanzhou University Second Hospital, Lanzhou, People’s Republic of China; 2Department of Pharmacy, Lanzhou University Second Hospital, Lanzhou, People’s Republic of China

*These authors contributed equally to this work

Background: Curdione is one of the most highly concentrated component of the active constituents in E-zhu, which has been reported to possess a variety of activities. However, the pharmacologic neuroprotective activity of curdione has not been evaluated. The present study aimed to investigate the protective effect of curdione on focal cerebral ischemia reperfusion-induced injury in rats and further exploring the underlying mechanisms.
Materials and methods: Adult male Sprague Dawley rats were subjected to middle cerebral artery occlusion (MCAO) surgery for 2 h, followed by reperfusion stage. All animals received treatment once a day for 7 days before surgery and 14 days from 4 h after the reperfusion started. The neurological deficit test and Morris water maze test were performed at 1, 4, 7 and 14 days after MCAO. The infarct size of animals was determined by the 2,3,5-triphenyltetrazolium chloride staining, and pathological brain damage was estimated by hematoxylin–eosin staining. The malonaldehyde (MDA) levels and the activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-PX) were detected by enzyme-linked immunosorbent assay. Expression of apoptotic proteins was measured by Western blot.
Results: Our results showed that curdione could significantly reduce the infarct size and neurological deficits, promote cognitive function recovery and recover neuronal morphologic damages in MCAO rats. It also blocked the increase of MDA content and elevated the activities of SOD, CAT and GSH-PX. Moreover, curdione attenuated the expression of Cyt-C, c-caspase-3 and c-caspase-9 increased the Bcl-2/Bax ratio and hence decreased the cellular apoptosis.
Conclusion: Curdione possessed potential neuroprotective effect on rats in the MCAO model. The anti-oxidative and anti-apoptotic properties may be involved in the underlying mechanisms.

Keywords: curdione, cerebral ischemia reperfusion, oxidative stress, apoptosis
 

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