The Neuroprotective Mechanism Of Interaction Between Interleukin 8 And Astrocytes During Local Cerebral Ischemia

Objective: To observe the change of GFAP expression in astrocytes and the effect of platelet- activating factor receptor antagonist ginkgolide B on GFAP expression during thrombotic cerebral ischemia in tree shrews. In addtion, we also investigate the relationship between IL-8 and neuronal viability and GFAP expression in astrocytes under cultured conddition.Methods: The focal thrombotic cerebral ischemia was induced by photochemical reaction in tree shrews. The absorbance of GFAP expression in astrocytes was detected by immunohistochemistry in different times after foci cerebral ischemia . After treating cultured cells with IL-8, the previous method and MTT method was used respectively to observe GFAP expression in astrocytes or neuronal viability.ResultstGFAP expression increased significantly(P<0.01) at 24h within astrocytes of penumbra and keeping high at 72h, whereas GFAP expression increased(P<0.05) at 72h within the distant of infarct and contralateral cortex after cerebral ischemia. GFAP expression decreased when the animals were given GB at 6h after thrombotic cerebral ischemia . After adding IL-8 into cultured cells, the neuronal viability and GFAP expression in astrocytes had nochange,but the number of GFAP(+) cells were increased marktly in dose- and time- dependent. Conclusions:GFAP which expression in astrocytes could ameliorate the microenvironment. But astrocytes dysfuntion and ischemic injury very sever so neuronal was damaged at 24h after local cerebral ischemia.The morphological change alleviated and GFAP expression keeping high in astrocytes at 72h after cerebral ischemia. The results of cell culture show that IL-8 would increase the number of astrocytes and do not scathe neurons.Present study suggested that the interaction between IL-8 and astrocytes could benefit neuroals after local cerebral ischemia. Neuroal necrosis would result in GFAP expression in astrocytes after local cerebral ischemia and GB could protect neurons by antagonizing PAF receptor and inhibit GFAP expression.There is different meshnism of GFAP expression between distant of infarct or contralateral cortex and penumbra after cerebral ischemia.