A number of membrane lipid-derived mediators play pivotal roles in the initiation, maintenance, and regulation of various types of acute and chronic pain. Acute pain, comprising nociceptive and inflammatory pain warns us about the presence of damage or harmful stimuli. However, it can be efficiently reversed by opioid analgesics and anti-inflammatory drugs. Prostaglandin E₂ and I₂, the representative lipid mediators, are well-known causes of acute pain. However, some lipid mediators such as lipoxins, resolvins or endocannabinoids suppress acute pain. Various types of peripheral and central neuropathic pain (NeuP) as well as fibromyalgia (FM) are representatives of chronic pain and refractory owing to abnormal pain processing distinct from acute pain. Accumulating evidence demonstrated that lipid mediators represented by lysophosphatidic acid (LPA) are involved in the initiation and maintenance of both NeuP and FM in experimental animal models. The LPAR₁-mediated peripheral mechanisms including dorsal root demyelination, Ca_vα2δ1 expression in dorsal root ganglion, and LPAR₃-mediated amplification of central LPA production via glial cells are involved in the series of molecular mechanisms underlying NeuP. This review also discusses the involvement of lipid mediators in emerging research directives, including itch-sensing, sexual dimorphism, and the peripheral immune system.

许多膜脂衍生介质在各种类型的急性和慢性疼痛的起始、维持和调节中起关键作用。急性疼痛，包括伤害性疼痛和炎症性疼痛，警告我们存在损伤或有害刺激。然而，它可以通过阿片类镇痛药和抗炎药有效地逆转。前列腺素 E ₂和 I ₂，代表脂质介质，是众所周知的急性疼痛的原因。然而，一些脂质介质如脂氧素、分解素或内源性大麻素可抑制急性疼痛。各种类型的外周和中枢神经性疼痛 (NeuP) 以及纤维肌痛 (FM) 是慢性疼痛的代表，并且由于与急性疼痛不同的异常疼痛处理而导致难治性疼痛。越来越多的证据表明，以溶血磷脂酸 (LPA) 为代表的脂质介质参与了实验动物模型中 NeuP 和 FM 的启动和维持。LPAR ₁介导的外周机制，包括背根脱髓鞘、背根神经节中的 Ca _v α2δ1 表达和 LPAR ₃通过神经胶质细胞介导的中枢 LPA 产生的扩增参与了 NeuP 的一系列分子机制。本综述还讨论了脂质介质在新兴研究方向中的作用，包括瘙痒感、性二态性和外周免疫系统。