Neuroprotective effects and mechanism of phycocyanin in cerebral ischemia reperfusion injury in rats / 中国海洋药物

ABSTRACT

Objective To investigate the neuroprotective effects and mechanism of phycocyanin in cerebral ischemia reperfusion injury in rats.Methods The model of middle cerebral artery occlusion reperfusion(MCAO/R) was established using the intraluminal filament occlusion with healthy adult male Wistar rats treated by phycocyanin.The apoptosis and the expression of bFGF and FGFR-1,IGF-1 and IGF-1R,iNOS and SOD were respectively determined by TUNEL and immunohistochemical staining to evaluate the effects of phycocyanin on above indexes.Results ① The rats showed neurobehavioral function disorders and the number of nerve cells reduced while apoptotic cells increased in ischemic area after ischemic reperfusion.In phycocyanin group,the number of apoptotic cells reduced siginificantly during reperfusion 12h~3d and the neurobehavioral function was better than that those in control group during reperfusion 7~14d.② In control group,the expressions of bFGF and FGFR-1 increased successfully from reperfusion 6h and reached a maximum at 1d,then subsided gradually in cortex and striatum.In phycocyanin group,the numbers of bFGF and FGFR-1 positive cells were higher than those in control group at the same time-points,which were significantly at reperfusion 1d and 12h~3d respectively.③ The expressions of IGF-1 and IGF-1R increased in cortex and striatum following cerebral ischemic and reperfusion.In phycocyanin group,the numbers of IGF-1 and IGF-1R positive cells in each time-point were higher than those in control group,which was significantly during reperfusion 6h~1d.④ In cotex and striatum,the iNOS and SOD expressed strongly and keep high level during 6h~7d with the maximum at reperfusion 1d.In phycocyanin group,iNOS expressed significantly higher during 12h~1d whlie SOD lower during 6h~1d than those in control group at the same time-point.Conclusion Phycocyanin might play a intrinsic antioxide effect by up-regulating SOD and down-regulating iNOS to inhibit neuronal apoptosis,and enhance the neuronal repairation by means of inducing the expressions of bFGF and IGF-1 following cerebral ischemic reperfusion in rats.