PDF(Pubmed)
Abstract：
Nerve injury is a common condition that occurs as a result of trauma, iatrogenic injury, or long-lasting stimulation. Unlike the central nervous system (CNS), the peripheral nervous system (PNS) has a strong capacity for self-repair and regeneration. Peripheral nerve injury results in the degeneration of distal axons and myelin sheaths. Macrophages and Schwann cells (SCs) can phagocytose damaged cells. Wallerian degeneration (WD) makes the whole axon structure degenerate, creating a favorable regenerative environment for new axons. After nerve injury, macrophages, neutrophils and other cells are mobilized and recruited to the injury site to phagocytose necrotic cells and myelin debris. Pro-inflammatory and anti-inflammatory factors involved in the inflammatory response provide a favorable microenvironment for peripheral nerve regeneration and regulate the effects of inflammation on the body through relevant signaling pathways. Previously, inflammation was thought to be detrimental to the body, but further research has shown that appropriate inflammation promotes nerve regeneration, axon regeneration, and myelin formation. On the contrary, excessive inflammation can cause nerve tissue damage and pathological changes, and even lead to neurological diseases. Therefore, after nerve injury, various cells in the body interact with cytokines and chemokines to promote peripheral nerve repair and regeneration by inhibiting the negative effects of inflammation and harnessing the positive effects of inflammation in specific ways and at specific times. Understanding the interaction between neuroinflammation and nerve regeneration provides several therapeutic ideas to improve the inflammatory microenvironment and promote nerve regeneration.
摘要：
神经损伤是由于创伤而发生的常见病，医源性损伤,或持久的刺激。与中枢神经系统（CNS）不同，周围神经系统（PNS）具有很强的自我修复和再生能力。周围神经损伤导致远端轴突和髓鞘变性。巨噬细胞和雪旺细胞（SCs）可以吞噬受损的细胞。瓦勒变性（WD）使整个轴突结构退化，为新轴突创造良好的再生环境.神经损伤后,巨噬细胞，中性粒细胞和其他细胞被动员并募集到损伤部位，吞噬坏死细胞和髓鞘碎片。参与炎症反应的促炎和抗炎因子为周围神经再生提供了良好的微环境,并通过相关信号通路调节炎症对机体的影响。以前,炎症被认为对身体有害，但进一步的研究表明，适当的炎症促进神经再生，轴突再生,和髓鞘形成。相反,过度炎症可引起神经组织损伤和病理变化,甚至导致神经系统疾病。因此,神经损伤后，体内的各种细胞与细胞因子和趋化因子相互作用，通过抑制炎症的负面影响，并在特定的方式和特定的时间利用炎症的积极作用来促进周围神经的修复和再生。了解神经炎症与神经再生之间的相互作用为改善炎症微环境和促进神经再生提供了几种治疗思路。
