Music Granule Ischemic Tolerance And Its Mechanism Of Experimental Research

Objective : To study the expression of Glial fibrillary acidic protein ( GFAP ) , Neuron-specific enolase (NSE), Neurotrophic factor (BDNF and bFGF) and Tumor necrosis factor-alpha (TNF-a ) in the ischemic tolerance induced by focal cerebral ischemic preconditioning, and to explore the mechanisms of ischemic tolerance. Furthermore, to investigate whether the Le-Mai-keli(LM) could enhance the ischemic tolerance induced by focal cerebral ischemic preconditioning.Methods: In this study, Ischemic preconditioning (IP) was induced by intraluminal filament middle cerebral artery for 10 min. Middle cerebral artery occlusion (MCAO) was induced by intraluminal filament for 2h after IP 72h. 60 SD rats were included and randomly divided into 3 groups: Control group (SS+MCAO) only received 2h MCAO followed by 22h reperfusion with pretreatment of sham surgery 3d before, focal ischemic preconditioning group (IP+MCAO) received 2h MCAO followed by 22h reperfusion with IP, and IP+LM+MCAO group received 2h MCAO followed by 22h reperfusion with IP and GY administration through esophagus twice a day. Each group was 20 SD rats. At 22h perfusion end point, the neurologic deficit score and infarct volume, histopathological changes with HE staining under a microscopy and an electron microscopy, and the expression of GFAP, NSE, BDNF, bFGF and TNF-a by using immunohistochemistry method were evaluated in each group. Results : (1)The neurologic deficit scores of the IP+MCAO group and IP+LM+MCAO group were significantly reduced than that of the SS+MCAO group, but in the IP+LM+MCAO group reduced moresignificantly than that in the IP+MCAO group . The infarct volume and the apoptosis neuron number of IP+LM+MCAO group were significantly less than that in the IP+MCAO group (P<0.05)and in the SS+MCAO group (PO.05). The pathological change was mild detected in the brain of IP+LM+MCAO group, and moderate detected in the brain of IP+MCAO group. ?The number of GFAP and NSE positive cells in the brain of SS+MCAO group, in which the morphological changes of astrocytes were detected, were significantly less than that in the IP+MCAO group (P<0.05). However, the number of immunopositive cells in the GFAP and NSE staining in the brain of IP+LM+MCAO group were significantly increased than that in the IP+MCAO group (P<0.05).(3)Neurotrophic factors: Compared with the SS+MCAO group, theexpression of BDNF and bFGF increased significantly in the othergroups . Among them the most dramatic up-regulation of BDNFand bFGF were observed in the IP+LM+MCAO group. Thedifference among the three groups have significance with P<0.05.(4) Tumor necrosis factor-alpha(TNF-a): The expression of TNF-awas observed in the three groups. In contrast with SS+MCAOgroup, the expression of TNF-a was down-regulated significantlyin the IP+MCAO group and the further down-regulation wereobserved in the IP+LM+MCAO group.Conclusions :?Focal cerebral ischemic preconditioning can provide brainprotection and induce ischemic tolerance. ?Activating Astrocyte and up-regulation of the expression of neurotrophic factor and down-regulation of tumor necrosis factor-alpha might play important roles in the induction ofendogenous neuroprotection in the ischemic tolerance.(3)The Le-Mai-keli enchances the ischemic tolerance inducedby Focal cerebral ischemic preconditioning...