Neuroinflammation, an inflammatory response within the nervous system, has been shown to be implicated in the progression of various neurodegenerative diseases. Recent in vivo studies showed that lipopolysaccharide (LPS) preconditioning provides neuroprotection by activating Toll-like receptor 4 (TLR4), one of the members for pattern recognition receptor (PRR) family that play critical role in host response to tissue injury, infection, and inflammation. Pre-exposure to low dose of LPS could confer a protective state against cellular apoptosis following subsequent stimulation with LPS at higher concentration, suggesting a role for TLR4 pre-activation in the signaling pathway of LPS-induced neuroprotection. However, the precise molecular mechanism associated with this protective effect is not well understood. In this article, we provide an overall review of the current state of our knowledge about LPS preconditioning in attenuating apoptosis mechanism and conferring neuroprotection via TLR4 signaling pathway.

神经炎症是神经系统内的一种炎症反应，已被证明与各种神经退行性疾病的进展有关。最近的体内研究表明，脂多糖 (LPS) 预处理通过激活 Toll 样受体 4 (TLR4) 提供神经保护，TLR4 是模式识别受体 (PRR) 家族的成员之一，在宿主对组织损伤、感染和感染的反应中起关键作用。炎。预先暴露于低剂量的 LPS 可以在随后用更高浓度的 LPS 刺激后赋予细胞凋亡保护状态，表明 TLR4 预激活在 LPS 诱导的神经保护信号通路中的作用。然而，与这种保护作用相关的精确分子机制尚不清楚。在本文中，