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RESEARCH ARTICLE
Year : 2020  |  Volume : 15  |  Issue : 3  |  Page : 548-556

Neuroprotection of Cyperus esculentus L. orientin against cerebral ischemia/reperfusion induced brain injury


1 Yingdong College of Food Science and Engineering, Shaoguan University, Shaoguan, Guangdong Province, China
2 School of Bioengineering, Jiangnan University, Wuxi, Jiangsu Province, China
3 Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX, USA
4 College of Life Sciences and Technology, Xinjiang University, Urumqi, Xinjiang Uygur Autonomous Region, China

Correspondence Address:
Liang-Jun Yan
Department of Pharmaceutical Sciences, UNT System College of Pharmacy, University of North Texas Health Science Center, Fort Worth, TX
USA
Si-Qun Jing
Yingdong College of Food Science and Engineering, Shaoguan University, Shaoguan, Guangdong Province
China
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Source of Support: This work was supported by the National Natural Science Foundation of China, No. 31770385 (to SQJ), Conflict of Interest: None


DOI: 10.4103/1673-5374.266063

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Orientin is a flavonoid monomer. In recent years, its importance as a source of pharmacological active substance is growing rapidly due to its properties such as anti-myocardial ischemia, anti-apoptosis, anti-radiation, anti-tumor, and anti-aging. However, the neuroprotective effects of Orientin on stroke injury have not been comprehensively evaluated. The aim of the present study was thus to investigate the neuroprotective capacity and the potential mechanisms of Cyperus esculentus L. orientin (CLO) from Cyperus esculentus L. leaves against ischemia/reperfusion (I/R) injury using standard orientin as control. For in vitro studies, we treated HT22 cells with CoCl2 as an in vitro ischemic injury model. HT22 cells in the control group were treated with CoCl2. For in vivo studies, we used rat models of middle cerebral artery occlusion, and animals that received sham surgery were used as controls. We found that CLO protected CoCl2-induced HT22 cells against ischemia/reperfusion injury by lowering lipid peroxidation and reactive oxygen species formation as well as decreasing protein oxidation. However, CLO did not reduce the release of lactate dehydrogenase nor increase the activity of superoxide dismutase. Results showed that CLO could decrease neurological deficit score, attenuate brain water content, and reduce cerebral infarct volume, leading to neuroprotection during cerebral ischemia-reperfusion injury. Our studies indicate that CLO flavonoids can be taken as a natural antioxidant and bacteriostastic substance in food and pharmaceutical industry. The molecular mechanisms of CLO could be at least partially attributed to the antioxidant properties and subsequently inhibiting activation of casepase-3. All experimental procedures and protocols were approved on May 16, 2016 by the Experimental Animal Ethics Committee of Xinjiang Medical University of China (approval No. IACUC20160516-57).


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