INFLUENCE OF NEUREGULIN ON NEURONAL APOPTOSIS AND EXPRESSIONS OF STAT3 AND GFAP FOLLOWING CEREBRAL ISCHEMIC REPERFUSION INJURY IN RATS
Yunliang Guo
Abstract
Yunliang Guo
Abstract
Objective To observe the influence of neuregulin-1β(NRG-1β) on neuronal apoptosis and the expressions of signal transducer and activator of transcription(STAT3) and glial fiberillary acidic protein(GFAP) following cerebral ischemia/reperfusion in rats.Methods The animal models of middle cerebral artery occlusion/reperfusion(MCAO/R) was established by the intralumianl filament method from left external-internal carotid artery in adult healthy male Wistar rats.The rat models were treated by injecting 1.5% NRG-1β 5μl from internal carotid artery.The neuronal apoptosis was detected by DendEnd fluorometric TUNEL assay,and the expressions of STAT3 and GFAP were determined by immunohistochemical and immumofluorescent assays.Results The cerebral ischemia/reperfusion injury could induce neuronal apoptosis and the expressions of STAT3 and GFAP in brain tissue.In control group,the number of neuronal apoptosis increased gradually and the STAT3 and GFAP were expressed highly along ischemia times in the cortex,striatum and hippocampus areas.After treatment with NRG-1β,the number of neuronal apoptosis reduced and the expression level of STAT3 and GFAP increased when compared to those in the control group at different ischemia times and corresponding areas(P0.05).Conclusion NRG-1β might play a neuroprotective role in cerebral iscehemia injury by activating JAK/STAT signal transduction pathway,thus promoting astrogliosis and regulating the anti-appoptosis mechanism of neural cells.
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Objective To observe the influence of neuregulin-1β(NRG-1β) on neuronal apoptosis and the expressions of signal transducer and activator of transcription(STAT3) and glial fiberillary acidic protein(GFAP) following cerebral ischemia/reperfusion in rats.Methods The animal models of middle cerebral artery occlusion/reperfusion(MCAO/R) was established by the intralumianl filament method from left external-internal carotid artery in adult healthy male Wistar rats.The rat models were treated by injecting 1.5% NRG-1β 5μl from internal carotid artery.The neuronal apoptosis was detected by DendEnd fluorometric TUNEL assay,and the expressions of STAT3 and GFAP were determined by immunohistochemical and immumofluorescent assays.Results The cerebral ischemia/reperfusion injury could induce neuronal apoptosis and the expressions of STAT3 and GFAP in brain tissue.In control group,the number of neuronal apoptosis increased gradually and the STAT3 and GFAP were expressed highly along ischemia times in the cortex,striatum and hippocampus areas.After treatment with NRG-1β,the number of neuronal apoptosis reduced and the expression level of STAT3 and GFAP increased when compared to those in the control group at different ischemia times and corresponding areas(P0.05).Conclusion NRG-1β might play a neuroprotective role in cerebral iscehemia injury by activating JAK/STAT signal transduction pathway,thus promoting astrogliosis and regulating the anti-appoptosis mechanism of neural cells.
Key concepts: Astrogliosis, Ischemia, Apoptosis, TUNEL assay, STAT protein, Glial fibrillary acidic protein, Medicine, STAT3