目的 研究姜黃素對化學缺氧所致人源性神經(jīng)星形膠質(zhì)瘤細胞系U87炎癥反應(yīng)的影響，并探討相關(guān)分子機制。方法 100 μmol/L CoCl₂處理U87細胞不同時間（1、3、6、12、24 h），實時熒光定量PCR（qRT-PCR）法檢測炎癥因子白細胞介素-1β（IL-1β）、白細胞介素-6（IL-6）、腫瘤壞死因子-α（TNF-α） mRNA表達變化。100 μmol/L CoCl₂處理U87細胞12 h制備化學缺氧模型，同時給予1、5和10 μmol/L姜黃素處理，對照組（不添加CoCl₂）和模型組給予等體積DMSO；qRTPCR法檢測IL-1β、IL-6、TNF-α mRNA表達變化；Western Blotting法檢測NF-κB/P65蛋白磷酸化水平及核轉(zhuǎn)位。結(jié)果 CoCl₂上調(diào)U87細胞IL-1β、IL-6、TNF-α mRNA水平并呈時間相關(guān)性，炎癥反應(yīng)在約12 h達到高峰。與模型組比較，姜黃素顯著下調(diào)炎癥因子IL-1β、IL-6和TNF-α的mRNA水平，5和10 μmol/L濃度組差異顯著（P<0.05）；顯著下調(diào)p65的磷酸化水平（P<0.05）；導致細胞核內(nèi)NF-κB/p65蛋白顯著減少、細胞質(zhì)中NF-κB/p65蛋白顯著增加（P<0.05）。結(jié)論 姜黃素通過下調(diào)NF-κB信號通路抑制化學缺氧誘導的U87細胞炎癥反應(yīng)。

Objective to investigate effects of traditional Chinese herbal extract monomer- curcumin (Cur) on astrocyte inflammation induced by hypoxia.Methods cobalt chloride (CoCl₂) was applied to the astrocyte cell line U87 resulting in cellular hypoxia. The changes of inflammatory cytokines after hypoxia and Cur treatment were determined by real-time reverse transcription polymerase chain reaction. The effects of Cur on NF - κB signaling pathway and nuclear translocation in hypoxic U87 cells were studied by Western Blotting. Results CoCl₂ up-regulated the transcriptional level of astrocyte inflammatory cytokines in a dose-dependent manner, and Cur significantly inhibited inflammation of astrocyte induced by chemical hypoxia. CoCl₂-induced chemical hypoxia lead to increased phosphorylation of p65 in the cytosol and promotes nuclear translocation of p65. Cur pretreatment significantly inhibited the activation of the above signaling pathway. Conclusion Cur exerts neuroprotective effects by inhibiting NF-κB signaling pathway and down-regulation of astrocyte inflammation induced chemical hypoxia.