The protective effect and its mechanism of 3-n-butylphthalide pretreatment on cerebral ischemia reperfusion injury in rats

• Published in: European review for medical and pharmacological sciences Vol. 21; no. 22; p. 5275
• Main Authors: Yan, R-Y, Wang, S-J, Yao, G-T, Liu, Z-G, Xiao, N
• Format: Journal Article
• Language: English
• Published: Italy 01.11.2017
• Subjects: Animals; Apoptosis - drug effects; Benzofurans - therapeutic use; Blood-Brain Barrier - drug effects; Body Water - metabolism; Brain Ischemia - prevention & control; Caspase 3 - biosynthesis; Hippocampus - drug effects; Hippocampus - metabolism; Infarction, Middle Cerebral Artery - complications; Infarction, Middle Cerebral Artery - pathology; Malondialdehyde - metabolism; MAP Kinase Signaling System - drug effects; Neurons - drug effects; Neuroprotective Agents - therapeutic use; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species - metabolism; Reperfusion Injury - prevention & control; Superoxide Dismutase - metabolism
• ISSN: 2284-0729
• DOI: 10.26355/EURREV_201711_13852

To investigate the potential effect of 3-n-butylphthalide (NBP) pretreatment on the cerebral ischemia/reperfusion injury in rats and the relevant mechanism. A total of 90 rats was divided into three groups: Sham operation group (Sham group), ischemia-reperfusion group (I-R group), and NBP pretreatment group (NBP group 75 mg·kg-1·d-1 gavage). Pre-treatment was given once a day within 1 week before establishing the rat model of cerebral ischemia-reperfusion injury. The middle cerebral artery occlusion (MACO) rat models were established with the improved Longa-Zea method on the 7th day after ischemia for 2 h and reperfusion for 24 h in all the rats. We detected the cerebral infarction, the pathologic change of brain, the apoptosis of nerve cell, the production levels of reactive oxygen species (ROS), the content of malonaldehyde (MDA) and the activity of superoxide dismutase (SOD), the water content and the permeability of blood-brain barriers (BBB). In addition, we also observed the expressions of mitogen-activated protein kinase (MAPK, p-38, JNK, ERK1/2) and cleaved caspase-3 in the hippocampus tissues. Compared with Sham group, we discovered that NBP significantly reduced infarction area, cell apoptosis, BBB damage and water content. Further, we found that NBP could also decrease ROS and MDA, and increase SOD activity in brain tissues of rats with a cerebral ischemia-reperfusion injury. Moreover, results showed that NBP also inhibited the levels p38 and JNK. NBP protected the cerebral from I/R injury, providing ideas for the expansion of clinical adaptability of NBP and possible approaches for its application.