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山奈酚可减轻神经炎症和血脑屏障功能障碍,改善脑缺血/再灌注大鼠的神经功能缺损。

Kaempferol attenuates neuroinflammation and blood brain barrier dysfunction to improve neurological deficits in cerebral ischemia/reperfusion rats.

机构信息

State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China; Beijing Key Laboratory of Drug Target Identification and New Drug Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.

Beijing Key Laboratory of Drug Target Identification and New Drug Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100050, China.

出版信息

Brain Res. 2019 Nov 1;1722:146361. doi: 10.1016/j.brainres.2019.146361. Epub 2019 Aug 1.

Abstract

Kaempferol has been reported to act as an anti-inflammatory agent in LPS-induced neuroinflammation in vitro and in vivo, but its role in the inflammation after cerebral ischemia/reperfusion (I/R) is unclear. The present study was to investigate the effect of kaempferol on inflammation in ischemic brain tissue and explore its mechanisms in cerebral I/R rats. Cerebral I/R rat model was established by middle cerebral artery occlusion for 60 min and following reperfusion. Kaempferol at doses of 25, 50 and 100 mg/kg was administered for 7 days after cerebral I/R. Kaempferol treatment significantly reduced cerebral infarct volume, attenuated inflammation and blood-brain barrier (BBB) disruption after cerebral I/R, thus improved neurological outcomes at the day 7 after cerebral I/R. Furthermore, the results also showed kaempferol treatment decreased the phosphorylation and nuclear transposition of transcription factor NF-κB p65, thus inhibited expression of various pro-inflammatory proteins. In conclusion, kaempferol attenuates neuroinflammation and blood brain barrier dysfunction to improve neurological deficits in cerebral I/R rats, its mechanism is related to NF-κB pathway.

摘要

山柰酚已被报道在体外和体内的 LPS 诱导的神经炎症中作为一种抗炎剂发挥作用,但它在脑缺血/再灌注(I/R)后的炎症中的作用尚不清楚。本研究旨在探讨山奈酚对缺血性脑组织炎症的影响,并探讨其在脑 I/R 大鼠中的作用机制。通过大脑中动脉闭塞 60min 并随后再灌注来建立脑 I/R 大鼠模型。在脑 I/R 后给予山奈酚 25、50 和 100mg/kg 剂量治疗 7 天。山奈酚治疗可显著降低脑梗死体积,减轻脑 I/R 后炎症和血脑屏障(BBB)破坏,从而改善脑 I/R 后第 7 天的神经功能结局。此外,结果还表明,山奈酚治疗可降低转录因子 NF-κB p65 的磷酸化和核易位,从而抑制各种促炎蛋白的表达。综上所述,山奈酚可减轻神经炎症和血脑屏障功能障碍,改善脑 I/R 大鼠的神经功能缺损,其机制与 NF-κB 通路有关。

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