Tropical Journal of Pharmaceutical Research

Original Research Article | OPEN ACCESS

Protective effect of grifolin against brain injury in an acute cerebral ischemia rat model

Shan Jing^1,2, Piaopiao Ying³, Xiaohua Hu², Ze Yu², Jianwei Sun², Yuchao Ding², Hongyan Du², Shuijiang Song⁴

¹Zhejiang University School of Medicine, Zhejiang 310058; ²Department of Neurological Rehabilitation, The Armed Police Corps Hospital In Hangzhou, Zhejiang Province, Zhejiang 310051; ³Clinical Laboratory, The Second Hospital Affiliated to Zhejiang University School of Medicine; ⁴Department of Neurology, The Second Hospital Affiliated to Zhejiang University School of Medicine, Zhejiang 310009, China.

For correspondence:- Shuijiang Song Email: shuijiangsong@hotmail.com Tel:+8657187783777

Received: 24 January 2017 Accepted: 19 May 2017 Published: 29 June 2017

Citation: Jing S, Ying P, Hu X, Yu Z, Sun J, Ding Y, et al. Protective effect of grifolin against brain injury in an acute cerebral ischemia rat model. Trop J Pharm Res 2017; 16(6):1299-1305 doi: 10.4314/tjpr.v16i6.13

© 2017 The authors.
This is an Open Access article that uses a funding model which does not charge readers or their institutions for access and distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0) and the Budapest Open Access Initiative (http://www.budapestopenaccessinitiative.org/read), which permit unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited..

Abstract

Purpose: To evaluate the protective effects of grifolin against brain injury in an acute cerebral ischemia rat model.

Methods: Rats were assigned to five groups: control, negative control, and grifolin (50, 100, and 200 mg/kg, p.o.) treated groups, which received the drug for 2 weeks. All the animals were sacrificed at the end of the protocol, and tissue homogenates were prepared from isolated brain tissue. Glutathione peroxidase (GPX), superoxide dismutase (SOD), malondialdehyde (MDA), and nitric oxide (NO), as oxidative stress indicators, were determined for the tissue homogenates of the ischemic rats. Inflammatory mediators (cytokines and nuclear factor kappa B p65, NF κB), DNA damage, and ATP and caspase 3 levels in the tissue homogenates were also assessed.

Results: Treatment with grifolin increased SOD and GPX significantly and decreased MDA and NO levels in tissue homogenates of the cerebral ischemic rats compared with those in the negative control group (p < 0.05). Treatment with grifolin also attenuated the altered levels of inflammatory mediators (cytokines and NF-κB), caspase 3, and ATP levels in the tissue homogenate of cerebral ischemic rats (p < 0.05). The results of comet assay on the tissue homogenate suggest that treatment with grifolin reduced or prevented damage.

Conclusions: The results show that treatment with grifolin protects against neuronal damage in acute cerebral ischemic rats via its anti-inflammatory and anti-oxidant properties.

Keywords: Neuroprotection, Cerebral ischemia, Brain injury, DNA, Grifolin, Anti-oxidant