Sheng W S, Hu S, Gekker G, Zhu S, Peterson P K, Chao C C
Minneapolis Medical Research Foundation, MN 55404, USA.
Arch Immunol Ther Exp (Warsz). 1997;45(5-6):359-66.
Endogenous opioid peptides play a variety of roles in the central nervous system (CNS) from development to immune modulation. These functions are mediated mostly via specific opioid receptors uniquely localized in different brain regions and cells. Exogenous opioids can influence and modulate neuronal and glial cell function via an opioid receptor mediated mechanism, leading to either protection or damage of the brain. Mechanisms underlying CNS opioid effects may be mediated via immune mediators, such as cytokines, beta-chemokines, and free radicals (i.e. reactive oxygen intermediates (ROI) and nitric oxide (NO)) produced by activated glial cells (microglia and astrocytes). In the pathogenesis of HIV-1 infection in drug addicts, opiates such as morphine have been postulated to promote the progression of this virus and the development of secondary opportunistic infections. Kappa opioid receptor (KOR) ligands, on the other hand, may play a neuroprotective role. Differences in species, age, sex, cell culture system, stimuli, opioid administration route, concentrations used, strain of infectious agents, and treatment regimes have contributed to many conflicting results in the field of opioid research. More studies are needed to delineate how opioids exert their effects on glial cells as well as neurons with the goal of finding new therapeutic approaches for neurodegenerative diseases, such as AIDS dementia.
从发育到免疫调节，内源性阿片肽在中枢神经系统（CNS）中发挥着多种作用。这些功能大多是通过独特地定位于不同脑区和细胞中的特定阿片受体介导的。外源性阿片类物质可通过阿片受体介导的机制影响和调节神经元及胶质细胞功能，从而导致对大脑的保护或损伤。中枢神经系统阿片类物质作用的潜在机制可能是通过免疫介质介导的，如细胞因子、β趋化因子以及由活化的胶质细胞（小胶质细胞和星形胶质细胞）产生的自由基（即活性氧中间体（ROI）和一氧化氮（NO））。在吸毒成瘾者的HIV-1感染发病机制中，吗啡等阿片类药物被认为会促进这种病毒的进展以及继发性机会性感染的发生。另一方面，κ阿片受体（KOR）配体可能发挥神经保护作用。物种、年龄、性别、细胞培养系统、刺激因素、阿片类药物给药途径、使用浓度、感染病原体的菌株以及治疗方案等方面的差异，导致了阿片类药物研究领域出现了许多相互矛盾的结果。需要更多的研究来阐明阿片类物质如何对胶质细胞以及神经元发挥作用，以期找到针对神经退行性疾病（如艾滋病痴呆）的新治疗方法。
