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Thrombopoietin could protect cerebral tissue against ischemia-reperfusion injury by suppressing NF-κB and MMP-9 expression in rats

Objective: To determine the neuroprotective effects and underpinning mechanisms of thrombopoietin (TPO), Matrix Metalloproteinase-9(MMP-9) and Nuclear Factor-κB (NF-κB) after focal cerebral ischemia-reperfusion in rats. Methods: Male rats underwent 2 hours of right middle cerebral artery occlusion (...

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Detalles Bibliográficos
Autores principales: Wu, Wenjuan, Zhong, Wei, Lang, Bing, Hu, Zhiping, He, Jialin, Tang, Xiangqi
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Ivyspring International Publisher 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6158660/
https://www.ncbi.nlm.nih.gov/pubmed/30275761
http://dx.doi.org/10.7150/ijms.27543
Descripción
Sumario:Objective: To determine the neuroprotective effects and underpinning mechanisms of thrombopoietin (TPO), Matrix Metalloproteinase-9(MMP-9) and Nuclear Factor-κB (NF-κB) after focal cerebral ischemia-reperfusion in rats. Methods: Male rats underwent 2 hours of right middle cerebral artery occlusion (MCAO) followed by 22 hours of reperfusion. PBS or TPO (0.1ug/kg) was administered from caudal vein before reperfusion. Neurologic deficits, brain edema, Evans blue (EB) extravasation, NF-κB and MMP-9 expression were subsequently examined. Results: Ischemia-reperfusion injury produced a large area of edema. TPO significantly reduced edema and alleviated neurologic deficits after ischemia-reperfusion. Ischemia-induced increases of NF-κB, MMP-9 and Evans blue extravasation were reduced by TPO intervention. Conclusion: TPO improved neurological function and ameliorated brain edema after stroke, partly by reducing the ischemia-induced increase of NF-κB and MMP-9.