【文獻解讀】

小膠質(zhì)細胞是中樞神經(jīng)系統(tǒng)中的常駐巨噬細胞樣細胞，可以通過極化為抗炎M2表型來抑制神經(jīng)炎癥相關(guān)疾病。福建醫(yī)科大學與福建中醫(yī)藥大學的研究團隊在一項研究中偶然發(fā)現(xiàn)迷迭香酸可以促進小膠質(zhì)細胞極化為M2表型。于是2020年9月，他們設(shè)計試驗研究迷迭香酸通過調(diào)節(jié)小膠質(zhì)細胞的極化來抑制神經(jīng)炎癥，并將相關(guān)結(jié)果發(fā)表于期刊《Inflammation Research》。

研究人員發(fā)現(xiàn)，在小鼠體外和體內(nèi)神經(jīng)炎癥條件下迷迭香酸都能抑制M1小膠質(zhì)細胞極化并促進小膠質(zhì)細胞極化為M2表型。接著他們發(fā)現(xiàn)，PDPK1/Akt/mTOR 通路通過迷迭香酸誘導的缺氧誘導因子降解促進小膠質(zhì)細胞極化為M2表型。線粒體呼吸增加是 M2 巨噬細胞抗炎反應的特征和要求，為了確定線粒體呼吸在迷迭香酸介導的小膠質(zhì)細胞極化到脂多糖處理的細胞中M2表型中的作用，他們測量了用迷迭香酸處理的細胞中線粒體 ATP 的產(chǎn)生。發(fā)現(xiàn)迷迭香酸介導的小膠質(zhì)細胞極化向 M2 表型的促進需要增加線粒體呼吸和代謝重編程，令人意外的是，缺氧誘導因子也參與迷迭香酸調(diào)節(jié)的線粒體呼吸和代謝重編程，以促進小膠質(zhì)細胞極化為M2表型。

注：M1小膠質(zhì)細胞極化并極化為M2表型的過程。

當前青少年學習壓力過大，睡眠不足，長時間用腦等就會對大腦產(chǎn)生一些不好的影響，若大腦出現(xiàn)炎癥，對學習無疑是重災難，這一研究結(jié)果，為消除大腦炎癥提供了一種新的潛在的治療方法。

【文獻節(jié)選】

Microglia are resident macrophage-like cells in the central nervous system (CNS). The induction of microglial activation dampens neuroinflammation-related diseases by promoting microglial (re)polarization to the anti-inflammatory (M2) phenotype and can serve as a potential therapeutic approach. Mitochondrial respiration and metabolic reprogramming are required for the anti-inflammatory response of M2 macrophages. However, whether these mitochondrial-dependent pathways are involved in microglial (re)polarization to the anti-inflammatory (M2) phenotype under conditions of lipopolysaccharide (LPS)induced neuroinflammation remains unclear. Moreover, the mechanisms that coordinate mitochondrial respiration and the functional reprogramming of microglial cells have not been fully elucidated. Rosmarinic acid (RA) possesses antioxidative and anti-inflammatory activities, and we previously reported that RA markedly suppresses LPS-stimulated M1 microglial activation in mice.