Effects of ginsenoside CK pretreatment on oxidative stress and inflammation in rats with cerebral ischemia/reperfusion injury

• Main Authors: Shuang Jiang, Haina Zhang, Min Qian, Xin Su, Xiaoqi Sun, Tianqi Wu, Wu Song
• Format: Article
• Language: English
• Published: Taylor & Francis Group 2018-11-01
• Series: Biotechnology & Biotechnological Equipment
• Subjects: Ginsenoside CK; cerebral ischemia/reperfusion; oxidative stress; inflammatory reaction; HMGB1
• Online Access: http://dx.doi.org/10.1080/13102818.2018.1525323

The prevention and treatment of cerebral ischemia/reperfusion injury has become a key link in the treatment of ischemic cerebrovascular diseases. In this study, Wistar rats were randomly divided into Sham, low-dose ginsenoside (L-CK), high-dose ginsenoside (H-CK) and nimodipine groups, and the rats in the L-CK, H-CK, and nimodipine groups were intragastrically given the corresponding agents successively once a day for 15 days before surgery. At 1 h after the last administration, a rat cerebral ischemia/reperfusion model was established by suture-occluded method and the effects of ginsenoside CK on the neurological scores, brain tissue water content, brain infarct volume, oxidative stress and inflammation were investigated. The results showed that, compared with those in the model group, the neurological behaviour scores in the L- and H-CK groups, the brain tissue water content in the H-CK group, and the brain infarct volume ratios in the L- and H-CK groups were significantly reduced. Compared with those in the model group, the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activities increased, whereas the malondialdehyde (MDA) content decreased significantly in the brain tissue of the rats in the L- and H-CK groups. Compared with that in the model group, the content of TNF-α in the H-CK group, the content of IL-1β and the expression of HMGB1 protein in the L- and H-CK groups were significantly reduced. These results suggest that ginsenoside CK can protect against cerebral ischemia reperfusion injury in rats, which may be related to its anti-oxidative, anti-inflammatory and HMGB1-expression inhibitory activity.