NM  Vol.2 No.4 , December 2011
The Neuroinflammatory Response Induced by PAF Can Be Attenuated by BN52021 Administration
Abstract: Objective: The purpose of this study was to determine whether BN52021, a platelet-activation factor receptor (PAFR) antagonist, could provide neuroprotection from the cytotoxic effects of PAF-induced neuroinflammation. Methods: The inflammagen platelet-activation factor (PAF) was first added to cultured PC12 cells. BN52021 was then added 24 hours later, survival rate and rate of apoptosis of the PC12 cells was determined by the MTT method and flow cytometry. In addition, PAF was injected into the fourth ventricle, and the effect of BN52021 administration was determined in rats. Results: PAF induced apoptosis in cultured PC12 cells, and BN52021 administration protected PC12 cells from PAF-induced apoptosis. When PAF is injected into the fourth ventricle, PAF induces acute neuroinflammation in the whole brain of rats. Acute PAF infusions also impaired spatial recognition in rats. The peripheral administration of BN52021 (i.p.) protected the rats from this impairment in spatial recognition. Conclusion: The PAFR antagonist BN52021 provides neuroprotection from the cytotoxic effects induced by the inflamagen PAF.
Cite this paper: nullR. Han, J. Hu and G. Su, "The Neuroinflammatory Response Induced by PAF Can Be Attenuated by BN52021 Administration," Neuroscience and Medicine, Vol. 2 No. 4, 2011, pp. 370-375. doi: 10.4236/nm.2011.24049.

[1]   X. D. Qu, R. Shrestha and M. D. Wang, “Risk Factors Analysis on Traumatic Brain Injury Prognosis,” Chinese Medical Sciences Journal, Vol. 26, No. 2, 2011, pp. 98-102. doi:10.1016/S1001-9294(11)60027-8

[2]   J. M. Simard, Z. Geng, S. K. Woo, S. Ivanova, et al., “Glibenclamide Reduces Inflammation, Vasogenic Edema, and Caspase-3 Activation after Subarachnoid Hemorrhage,” Journal of Cerebral Blood Flow & Metabolism, Vol. 29, No. 2, 2009, pp. 317-30. doi:10.1038/jcbfm.2008.120

[3]   R. L. Wood and N. A. Rutterford, “Demographic and Cognitive Predictors of Long-Term Psychosocial Outcome Following Traumatic Brain Injury,” Journal of the International Neuropsychological Society, Vol. 12, No. 3, 2006, pp. 350-358. doi:10.1017/S1355617706060498

[4]   W. L. Titsworth, N. K. Liu and X. M. Xu, “Role of Secretory Phospholipase a(2) in CNS Inflammation: Implications in Traumatic Spinal Cord Injury,” CNS Neurological Disorders—Drug Targets, Vol. 7, No. 3, 2008, pp. 254-269. doi:10.2174/187152708784936671

[5]   X. Zhou, J. Zhou, X. Li, C. Guo, et al., “GSK-3β Inhibitors Suppressed Neuroinflammation in Rat Cortex by Activating Autophagy in Ischemic Brain Injury,” Biochemical and Biophysical Research Communications, Vol. 411, No. 2, 2011, pp. 271-275. doi:10.1016/j.bbrc.2011.06.117

[6]   S. S. Dai and Y. G. Zhou, “Adenosine 2A Receptor: A Crucial Neuromodulator with Bidirectional Effect in Neuroinflammation and Brain Injury,” Review in the Neuroscience, Vol. 22, No. 2, 2011, pp. 231-239. doi:10.1515/RNS.2011.020

[7]   Y. Deng, W. Fang, Y. Li, et al., “Blood-Brain Barrier Breakdown by PAF and Protection by XQ-1H Due to Antagonism of PAF Effects,” European Journal of Pharmacology, Vol. 616, No. 1-3, 2009, pp. 43-47. doi:10.1016/j.ejphar.2009.06.017

[8]   T. Tokutomi, H. Maruiwa, M. Hirohata, et al., “Production of Platelet-Activating Factor by Neuronal Cells in the Rat Brain with Cold Injury,” Neurological Research, Vol. 23, No. 6, 2001, pp. 605-611. doi:10.1179/016164101101199081

[9]   H. S. Lustig, J. Chan and D. A. Greenberg, “Comparative Neurotoxic Potential of Glutamate, Endothelins, and Platelet-Activating Factor in Cerebral Cortical Cultures,” Neuroscience Letters, Vol. 139, No. 1, 1992, pp. 15-18. doi:10.1016/0304-3940(92)90847-Z

[10]   S. Ishii and T. Shimizu, “Platelet-Activating Factor (PAF) Receptor and Genetically Engineered PAF Receptor Mutant Mice,” Progress in Lipid Research, Vol. 391, 2000, pp. 41-48. doi:10.1016/S0163-7827(99)00016-8