Neuroprotective effects of LBP on brain ischemic reperfusion neurodegeneration

H.-B. Wang, Y.-X. Li, Y.-J. Hao, T.-F. Wang, Z. Lei, Y. Wu, Q.-P. Zhao, H. ang, L. Ma, J. Liu, C.-J. Zhao, Y.-X. Jiang, Y.-R. Wang, X.-y. DAI, W.-n. Zhang, T. Sun, J.-q. Yu

Department of Pharmacology, Ningxia Medical University, Yinchuan, China. yujq910315@163.com

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• Phytomedicine

AIM: The present study was conducted to investigate whether LBP had a protective effect on cerebral ischemic reperfusion injury and to determine the possible mechanisms.

MATERIALS AND METHODS: Male Kunming (KM) mice were used to make the model cerebral artery occlusion/reperfusion (MCAO/R). The behavioral test was used to measure neurological deficit scores for evaluation of ischemic reperfusion damage of brain. The change of electroencephalograph (EEG) was monitored by Model SMUP-E Bio-electric Signals Processing System. The infarction area of brain was assessed in brain slices with 2% solution of 2,3,5-triphenyl tetrazolium chloride (TTC). Spectrophotometric assay was used to determine the activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) and lactate dehydrogenase (LDH), contents of malondialdehyde (MDA) and adenosine triphosphate (ATP) of the brain.

RESULTS: The results showed that LBP at doses of 20 and 40 mg/kg markedly decreased the neurological deficit scores and the infarction area in MCAO/R mice. At the same time, LBP significantly decreased MDA content, and increased SOD, GSH-Px, CAT, LDH activities in ischemic reperfusion brain.

CONCLUSIONS: These suggest that LBP might act as a potential neuroprotective agent against the cerebral reperfusion-induced injury in the brain through reducing lipid peroxides, scavenging free radicals, and improving the energy metabolism.

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