A bioactive gypenoside (GP-14) alleviates neuroinflammation and blood brain barrier (BBB) disruption by inhibiting the NF-κB signaling pathway in a mouse high-altitude cerebral edema (HACE) model
文献类型:期刊论文
作者 | Ya-Nan Geng4,6; Jun-Li Yang3; Xiang Cheng6; Ying Han6; Feng Yan5; Cheng-Bo Wang3; Xiu-Fang Jiang6; Xian-Hua Meng3; Ming Fan4,6; Ming Zhao6 |
刊名 | International Immunopharmacology |
出版日期 | 2022 |
期号 | 107页码:108675 |
关键词 | Gypenoside Neuroinflammation Blood brain barrier High altitude cerebral edema NF-κB signaling pathway |
DOI | 10.1016/j.intimp.2022.108675 |
英文摘要 | Background: Neuroinflammation caused by peripheral lipopolysaccharides (LPS) under hypoxia is a key contributor to the development of high altitude cerebral edema (HACE). Our previous studies have shown that gypenosides and their bioactive compounds prevent hypoxia-induced neural injuries in vitro and in vivo. However, their effect on neuroinflammation-related HACE remains to be illustrated. The present study aimed to investigate the effects of GP-14 in HACE mouse model. Methods: HACE mice were treated with GP-14 (100 and 200 mg/kg) for 7 days. After the treatments, the level of serum inflammation cytokines and the transcription of inflammatory factors in brain tissue were determined. The activation of microglia, astrocyte and the changes of IgG leakage and the protein levels of tight junction proteins were detected. Furthermore, the inflammatory factors and nuclear factor-κB (NF-κB) signaling pathway in BV-2 cells and primary microglia were detected. Results: GP-14 pretreatment alleviated both the serum and neural inflammatory responses caused by LPS stimulation combined with hypobaric hypoxia exposure. In addition, GP-14 pretreatment inhibited microglial activation, accompanied by a decrease in the M1 phenotype and an increase in the M2 phenotype. Moreover, the disruption of the blood brain barrier (BBB) integrity, including increased IgG leakage and decreased expression of tight junction proteins, was attenuated by GP-14 pretreatment. Based on the BV-2 and primary microglial models, the inflammatory response and activation of the NF-κB signaling pathway were also inhibited by GP-14 pretreatment. Conclusion: Taken together, our results demonstrated that GP-14 exhibited prominent protective roles against neuroinflammation and BBB disruption in a mouse HACE model. GP-14 could be a potential choice for the treatment of HACE in the future. |
语种 | 英语 |
源URL | [http://ir.licp.cn/handle/362003/29304] |
专题 | 兰州化学物理研究所_中科院西北特色植物资源化学重点实验室/甘肃省天然药物重点实验室 |
通讯作者 | Ling-Ling Zhu |
作者单位 | 1.School of Pharmaceutical Sciences, University of South China 2.College of Life Sciences, Anhui Medical University 3.CAS Key Laboratory of Chemistry of Northwestern Plant Resources and Key Laboratory for Natural Medicine of Gansu Province, Lanzhou Institute of Chemical Physics, Chinese Academy of Sciences (CAS) 4.Beijing Institute of Brain Disorders, Laboratory of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Capital Medical University 5.Co-Innovation Center of Neuroregeneration, Nantong University 6.Beijing Institute of Basic Medical Sciences |
推荐引用方式 GB/T 7714 | Ya-Nan Geng,Jun-Li Yang,Xiang Cheng,et al. A bioactive gypenoside (GP-14) alleviates neuroinflammation and blood brain barrier (BBB) disruption by inhibiting the NF-κB signaling pathway in a mouse high-altitude cerebral edema (HACE) model[J]. International Immunopharmacology,2022(107):108675. |
APA | Ya-Nan Geng.,Jun-Li Yang.,Xiang Cheng.,Ying Han.,Feng Yan.,...&Ling-Ling Zhu.(2022).A bioactive gypenoside (GP-14) alleviates neuroinflammation and blood brain barrier (BBB) disruption by inhibiting the NF-κB signaling pathway in a mouse high-altitude cerebral edema (HACE) model.International Immunopharmacology(107),108675. |
MLA | Ya-Nan Geng,et al."A bioactive gypenoside (GP-14) alleviates neuroinflammation and blood brain barrier (BBB) disruption by inhibiting the NF-κB signaling pathway in a mouse high-altitude cerebral edema (HACE) model".International Immunopharmacology .107(2022):108675. |
入库方式: OAI收割
来源:兰州化学物理研究所
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