炎症因子参与神经病理性疼痛-抑郁共病的研究进展

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.

Inflammatory cytokines in comorbidity of neuropathic pain and depression

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.