中国中药杂志

2020, v.45(19) 4686-4691

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黄芩苷对缺氧复氧损伤的人脑微血管内皮细胞炎性反应及TLR4/NF-κB信号通路的影响
Effect of baicalin on inflammatory response and TLR4/NF-κB signaling pathway of human brain microvascular endothelial cell after hypoxia-reoxygenation injury

张业昊;苗兰;张鹏;刘光宇;刘建勋;
ZHANG Ye-hao;MIAO Lan;ZHANG Peng;LIU Guang-yu;LIU Jian-xun;Beijing Key Laboratory of Pharmacology of Chinese Materia Region, Institute of Basic Medical Sciences,Xiyuan Hospital, China Academy of Chinese Medical Sciences;

摘要(Abstract):

该研究以人脑微血管内皮细胞(human brain microvascular endothelial cell,HBMEC)氧糖剥夺(oxygen-glucose deprivation,OGD)模型,模拟脑缺血神经细胞损伤,观察炎性反应,并从抑制炎性反应的角度探讨治疗脑缺血/再灌注、改善记忆障碍的可能机制,对相关中药治疗脑缺血疾病具有借鉴意义。选择HBMEC在OGD损伤同时给予药物,4 h后复氧2 h,收集细胞上清,测定细胞上清炎性因子含量;免疫荧光法检测HBMEC细胞形态,及细胞内磷酸化核因子-κB(p-nuclear factor kappa-light-chain-enhancer of activated B,p-NF-κB)表达量,免疫印迹法检测细胞Toll样受体4(Toll like receptor 4, TLR4)、骨髓分化主要反应蛋白(myeloid differentiation primary response 88,MYD88)、p-NF-κB表达变化。实验结果发现,HBMEC缺氧后白细胞介素6(interleukin 6,IL-6)、IL-1α、IL-1β与肿瘤坏死因子-α(tumor necrosis factor-α,TNF-α)含量显著升高,黄芩苷可保护HBMEC,抑制p-NF-κB的核内转录,并能明显降低OGD损伤引起的HBMEC炎性因子的释放,抑制TLR4,MYD88,p-NF-κB的表达。研究提示,黄芩苷对OGD损伤的HBMEC具有明显的保护作用,抑制炎性反应,其保护作用机制可能与抑制TLR4相关信号通路有关。该研究从抑制炎性反应的角度探讨治疗脑缺血/再灌注、改善记忆障碍的可能机制,对相关中药治疗脑缺血疾病具有借鉴意义。
In this study, the oxygen-glucose deprivation(OGD) model in the human brain microvascular endothelial cell(HBMEC) was used to simulate the ischemic neuronal damage and observe the inflammatory response, explore the possible mechanisms for treating cerebral ischemia/reperfusion and improving memory impairment from the view point of inhibiting inflammatory response, which is of great reference significance for related Chinese medicine treatment of ischemic diseases. HBMECs were given with drugs at the same time of OGD injury, and reoxygenated for 2 h after 4 h treatment. Cell supernatant was then collected, and the inflammatory factors in cell supernatant were detected. Immunofluorescence assay was used to detect HBMECs morphology and expression of p-nuclear factor kappa-light-chain-enhancer of activated B(p-NF-κB); Western blot was used to detect expression changes of Toll like receptor 4(TLR4), myeloid differentiation primary response 88(MYD88) and p-NF-κB. The results showed that, after OGD modeling, the levels of interleukin 6(IL-6), IL-1α, IL-1β and tumor necrosis factor-α(TNF-α) were significantly increased; baicalin protected HBMEC, inhibited intranuclear transcription of p-NF-κB, significantly decreased HBMEC release of inflammatory factors caused by OGD injury, and inhibited the expression of TLR4, MYD88, and p-NF-κB. The studies suggested that baicalin had obvious protective effect on HBMECs damaged by OGD, and could inhibit inflammatory response. Its protection mechanism may be related to inhibiting TLR4 signaling pathways.

关键词(KeyWords): 黄芩苷;人脑微血管内皮细胞(HBMEC);炎性因子;氧糖剥夺(OGD);TLR4;NF-κB
baicalin;human brain microvascular endothelial cell(HBMEC);cytokines;oxygen-glucose deprivation(OGD);TLR4;NF-κB

Abstract:

Keywords:

基金项目(Foundation): 中国中医科学院自主选题研究项目(ZZ11-068);; 国家自然科学基金项目(81903841)

作者(Author): 张业昊;苗兰;张鹏;刘光宇;刘建勋;
ZHANG Ye-hao;MIAO Lan;ZHANG Peng;LIU Guang-yu;LIU Jian-xun;Beijing Key Laboratory of Pharmacology of Chinese Materia Region, Institute of Basic Medical Sciences,Xiyuan Hospital, China Academy of Chinese Medical Sciences;

Email:

DOI: 10.19540/j.cnki.cjcmm.20200511.401

参考文献(References):

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