Sequences of the primers used for RT-qPCR.

Phosphatidylcholine (PC), a choline-containing phospholipid abundant in chicken eggs, is widely consumed as a dietary supplement. Epidemiological studies suggest that PC intake may improve cognitive function in patients with neurodegenerative diseases such as Alzheimer’s disease, although the underlying mechanisms remain largely unclear. In this study, we investigated the anti-inflammatory effects of PC and its molecular mechanisms using an in vitro inflammation model involving lipopolysaccharide (LPS)-stimulated MG6 mouse microglial cells. PC significantly suppressed the LPS-induced expression of pro-inflammatory cytokines, including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Mechanistically, PC inhibited the phosphorylation of inhibitor kappa Bα (IκBα), thereby preventing the nuclear translocation of nuclear factor-κB (NF-κB). PC also reduced the phosphorylation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK), and suppressed the nuclear translocation of activator protein-1 (AP-1), composed of c-Fos and c-Jun. These findings indicate that PC attenuates LPS-induced microglial inflammation via the NF-κB and JNK/p38 MAPK signaling pathways. Given the proposed role of chronic neuroinflammation in the progression of neurodegenerative diseases, the anti-inflammatory properties of PC demonstrated here may provide new insights into its potential contribution to maintaining brain health.

磷脂酰胆碱（Phosphatidylcholine，PC）是一类含胆碱的磷脂，在鸡蛋中含量丰富，常作为膳食补充剂被广泛摄入。流行病学研究表明，摄入磷脂酰胆碱或许可改善阿尔茨海默病等神经退行性疾病患者的认知功能，但其具体作用机制目前仍不完全明确。在本研究中，我们采用脂多糖（lipopolysaccharide，LPS）诱导的小鼠小胶质细胞MG6炎症体外模型，探究了磷脂酰胆碱的抗炎作用及其分子机制。实验结果显示，磷脂酰胆碱可显著抑制脂多糖诱导的促炎细胞因子表达，包括肿瘤坏死因子-α（tumor necrosis factor-α，TNF-α）、白细胞介素-1β（interleukin-1β，IL-1β）以及白细胞介素-6（interleukin-6，IL-6）。从分子机制来看，磷脂酰胆碱可抑制核因子κB抑制蛋白α（inhibitor kappa Bα，IκBα）的磷酸化，从而阻断核因子κB（nuclear factor-κB，NF-κB）的核转位过程。此外，磷脂酰胆碱还可降低c-Jun氨基末端激酶（c-Jun N-terminal kinase，JNK）与p38丝裂原活化蛋白激酶（mitogen-activated protein kinase，MAPK）的磷酸化水平，并抑制由c-Fos和c-Jun组成的激活蛋白-1（activator protein-1，AP-1）的核转位。上述研究结果表明，磷脂酰胆碱可通过核因子κB以及c-Jun氨基末端激酶/p38丝裂原活化蛋白激酶信号通路，缓解脂多糖诱导的小胶质细胞炎症反应。鉴于慢性神经炎症在神经退行性疾病进展中的潜在作用，本研究证实的磷脂酰胆碱抗炎特性，或为其在维持大脑健康方面的潜在价值提供全新的研究视角。