Department of Clinical Laboratory Sciences, Kufa University, Najaf, Iraq.
Department of Chemistry, College of Science, University of Kufa, Iraq.
Eur Psychiatry. 2019 Apr;57:46-51. doi: 10.1016/j.eurpsy.2018.10.001. Epub 2019 Jan 21.
Activation of the immune-inflammatory response system (IRS) and the compensatory immune-regulatory system (CIRS) and aberrations in endogenous opioids play a role in the pathophysiology of major depressive disorder (MDD). There are no studies which examined the associations between both systems in MDD. The aim of the present study was to examine the relation between β-Endorphin (β-EP), Endomorphin-2, and their mu-opioid receptor (MOR) as well as interleukin (IL)-6 and IL-10, an anti-inflammatory cytokine, in MDD patients.
The study included 60 depressed drug-free male patients and 30 matched controls. Serum β-EP, Endomorphin-2, MOR, IL-6 and IL-10 levels were measured using ELISA techniques.
The results revealed a significant increase in serum β-EP, MOR, IL-6 and IL-10 in MDD patients versus healthy controls. MOR levels were strongly associated with IL-10 levels. There were no significant correlations between endogenous opioids and IL-6 and IL-10.
The results show that MOR levels may function as a possible component of the CIRS whilst there is no evidence that β-EP and EM-2 may modify the IRS. The significant correlation between MOR levels and IL-10 may be explained through central activation of the HPA-axis and increased B-cell numbers expressing MOR as a response to cytokine over-secretion in MDD.
免疫炎症反应系统(IRS)和代偿性免疫调节系统(CIRS)的激活以及内源性阿片系统的异常在重度抑郁症(MDD)的病理生理学中起作用。目前还没有研究检查 IRS 和 CIRS 之间的关联。本研究的目的是研究 MDD 患者β-内啡肽(β-EP)、内吗啡肽-2 及其μ-阿片受体(MOR)以及白细胞介素(IL)-6 和抗炎细胞因子 IL-10 之间的关系。
该研究包括 60 名未经药物治疗的男性抑郁症患者和 30 名匹配的对照组。使用 ELISA 技术测量血清β-EP、内吗啡肽-2、MOR、IL-6 和 IL-10 水平。
结果显示,MDD 患者的血清β-EP、MOR、IL-6 和 IL-10 水平明显高于健康对照组。MOR 水平与 IL-10 水平呈强相关。内源性阿片类物质与 IL-6 和 IL-10 之间无显著相关性。
结果表明,MOR 水平可能作为 CIRS 的一个可能组成部分,而β-EP 和 EM-2 可能不会改变 IRS。MOR 水平与 IL-10 之间的显著相关性可能通过 HPA 轴的中枢激活和 B 细胞数量的增加来解释,这些 B 细胞表达 MOR 是对 MDD 中细胞因子过度分泌的反应。