神经炎症
小胶质细胞
NF-κB
肿瘤坏死因子α
IκB激酶
炎症
一氧化氮
神经保护
αBκ
化学
癌症研究
NFKB1型
药理学
医学
免疫学
内科学
生物化学
转录因子
基因
作者
Xing Zhang,Qun Liu,Lian Liu,Feng Qian,Bo Ren,Feng Ru Tang
标识
DOI:10.1177/15593258251382964
摘要
Background Radiation therapy for brain tumors often leads to radiation-induced brain injury, which is closely linked to microglial hyperactivation and neuroinflammation. Lycium barbarum polysaccharide (LBP), the primary active component of Lycium barbarum , may provide neuroprotection by suppressing microglial overactivation and reducing neuroinflammation. Methods BV2 microglial cells were pretreated with LBP for 12 hours (h), exposed to 10 Gy X-ray irradiation, and then post-treated with LBP for another 12 h. We assessed microglial polarization and measured levels of nitric oxide (NO), interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and key proteins in the IKKβ/IκBα/NF-κB pathway. Results LBP treatment shifted microglia from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype and significantly decreased the release of NO, IL-1β, and TNF-α following irradiation. Conclusion Our findings demonstrate that LBP mitigates radiation-induced microglial inflammation by inhibiting the IKKβ/IκBα/NF-κB pathway, suggesting its potential as a radioprotective agent against radiotherapy-induced neuroinflammation.
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