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Ephedrine attenuates cerebral ischemia/reperfusion injury in rats through NF-κB signaling pathway
Human & Experimental Toxicology ( IF 2.7 ) Pub Date : 2020-12-14 , DOI: 10.1177/0960327120975456
Chanhong Shi 1 , Jianhong Li 2 , Jianwei Li 3
Affiliation  

The inflammation and immune responses are critical in ischemic stroke and contribute to aggravated brain damage. Ephedrine was reported to play an important role in the control of inflammatory responses. This study was to investigate the repairing effects and potential mechanisms of ephedrine on cerebral ischemic injury in a rat model of focal cerebral ischemia. The rat model of cerebral ischemia/reperfusion injury was established using the middle cerebral artery occlusion (MCAO) method and then rats were treated with ephedrine (5 and 10 mg/kg) for 7 days. The neurobehavioral progression was assessed using the neurological scoring method. The pathology of brain tissue was evaluated by hematoxylin and eosin (H&E) staining. The infarct volume was examined by triphenyltetrazolium chloride (TTC) staining. The apoptosis in ischemic brain tissues was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). Gene quantification and protein expression were detected by real-time PCR and western blot, respectively. Ephedrine treatment significantly alleviated the cerebral ischemia/reperfusion injury, evidenced by decreased neurological deficit score, infarct volume and water content. Ephedrine also decreased autophagy and apoptosis in brain tissues. Moreover, ephedrine treatment significantly reduced inflammatory responses, associating with decreasing the protein expression of p-NF-κB. These results demonstrated neuroprotective properties of ephedrine and highlighted it as a new potential anti-inflammatory agent against injury of cerebral ischemia/reperfusion.



中文翻译:

麻黄碱通过NF-κB信号通路减轻大鼠脑缺血/再灌注损伤

炎症和免疫反应在缺血性中风中至关重要,并会导致脑损伤加重。据报道,麻黄碱在控制炎症反应方面发挥着重要作用。本研究旨在探讨麻黄碱对局灶性脑缺血模型大鼠脑缺血损伤的修复作用及潜在机制。采用大脑中动脉闭塞(MCAO)法建立大鼠脑缺血/再灌注损伤模型,然后给予麻黄碱(5和10mg/kg)治疗7天。使用神经学评分方法评估神经行为进展。通过苏木精和伊红 (H&E) 染色评估脑组织的病理学。通过氯化三苯基四唑鎓(TTC)染色检查梗塞体积。通过末端脱氧核苷酸转移酶 dUTP 缺口末端标记 (TUNEL) 法检测缺血性脑组织中的细胞凋亡。通过酶联免疫吸附试验(ELISA)检测炎症因子。基因定量和蛋白质表达分别通过实时 PCR 和蛋白质印迹检测。麻黄碱治疗显着减轻了脑缺血/再灌注损伤,表现为神经功能缺损评分、梗死体积和含水量降低。麻黄碱还能降低脑组织的自噬和细胞凋亡。此外,麻黄碱治疗显着降低了炎症反应,这与降低 p-NF-κB 的蛋白质表达有关。

更新日期:2020-12-14
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