目的 研究姜黃素對(duì)化學(xué)缺氧所致人源性神經(jīng)星形膠質(zhì)瘤細(xì)胞系U87炎癥反應(yīng)的影響，并探討相關(guān)分子機(jī)制。方法 100 μmol/L CoCl₂處理U87細(xì)胞不同時(shí)間（1、3、6、12、24 h），實(shí)時(shí)熒光定量PCR（qRT-PCR）法檢測(cè)炎癥因子白細(xì)胞介素-1β（IL-1β）、白細(xì)胞介素-6（IL-6）、腫瘤壞死因子-α（TNF-α） mRNA表達(dá)變化。100 μmol/L CoCl₂處理U87細(xì)胞12 h制備化學(xué)缺氧模型，同時(shí)給予1、5和10 μmol/L姜黃素處理，對(duì)照組（不添加CoCl₂）和模型組給予等體積DMSO；qRTPCR法檢測(cè)IL-1β、IL-6、TNF-α mRNA表達(dá)變化；Western Blotting法檢測(cè)NF-κB/P65蛋白磷酸化水平及核轉(zhuǎn)位。結(jié)果 CoCl₂上調(diào)U87細(xì)胞IL-1β、IL-6、TNF-α mRNA水平并呈時(shí)間相關(guān)性，炎癥反應(yīng)在約12 h達(dá)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(dǎo)致細(xì)胞核內(nèi)NF-κB/p65蛋白顯著減少、細(xì)胞質(zhì)中NF-κB/p65蛋白顯著增加（P<0.05）。結(jié)論 姜黃素通過(guò)下調(diào)NF-κB信號(hào)通路抑制化學(xué)缺氧誘導(dǎo)的U87細(xì)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.