炎症因子参与神经病理性疼痛抑郁共病的研究进展

Inflammatory cytokines in comorbidity of neuropathic pain and depression

背景 神经病理性疼痛与抑郁症共病严重影响了患者的生活质量。近年来研究发现，炎症因子在神经病理性疼痛？蛳抑郁共病发病中起重要作用。 目的 综述炎症因子参与神经病理性疼痛-抑郁共病的研究进展，为该病的有效防治提供参考 内容 神经病理性疼痛与感觉系统的功能障碍相关，它包括触诱发痛、痛觉过敏、自发痛等一系列疼痛症状。抑郁症表现为心境低落和厌恶活动。小胶质细胞激活后，释放的炎症因子如TNF-α、IL-6、IL-1β，通过结合5-羟色胺受体、谷氨酸盐受体、γ-氨基丁酸能受体及激活下丘脑-垂体-肾上腺素轴促进神经病理性疼痛和抑郁症的发生。 趋向 炎症因子可能是治疗神经病理性疼痛-抑郁共病的靶标。

Background Comorbidity of neuropathic pain and depression seriously affects life quality. Recent studies have found that cytokines play important roles in the pathogenesis of neuropathic pain-depression comorbidity. Objective To review the effects of inflammatory cytokines on neuropathic pain-depression comorbidity, which will provide clues for effective prevention and treatment of the comorbidity. Content Neuropathic pain is associated with injuries and dysfunctions of somatosensory nervous system, and consists of a series of pain symptoms, including allodynia, pain hypersensitivity, and spontaneous pain, etc. Depression is a state of low mood and aversion to activity. Following activation of microglia, many inflammatory cytokines, such as, TNF-α, IL-1β, and IL-6, elevate and subsequently exacerbate both neuropathic pain and depression by interacting with 5-HT receptors, glutamate receptors, γ-aminobutyric acid receptors, and promoting activation of hypothalamus-pituitary-adrenaline axis. Trend Inflammatory cytokines may be potential targets for the treatment of neuropathic pain-depression comorbidity.