Schipper H M, Liberman A, Stopa E G
Bloomfield Centre for Research in Aging, Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital, Montreal, Quebec, Canada.
Exp Neurol. 1998 Mar;150(1):60-8. doi: 10.1006/exnr.1997.6752.
Heme oxygenase-1 is a cellular stress protein expressed in brain and other tissues in response to oxidative challenge and other noxious stimuli. In the present study, immunohistochemistry was used to assess HO-1 expression in various postmortem human brain specimens derived from PD and control subjects. In the substantia nigra of both PD and control specimens, moderate HO-1 immunoreactivity was consistently observed in neuromelanin-containing (dopaminergic) neurons. Lewy bodies in PD nigra neurons exhibited intense HO-1 immunostaining in their peripheries. In both PD and control specimens, neuronal HO-1 staining was faint or nondetectable in the other brain regions surveyed. The fraction of GFAP-positive astroglia expressing HO-1 in PD substantia nigra (77.1 +/- 12.3) was significantly greater than that observed in the substantia nigra of control subjects (18.7 +/- 7.1; P = 0.0015). In the other regions examined, percentages of GFAP-positive astroglia coexpressing HO-1 were relatively low and did not differ significantly (P > 0.05) between control and PD specimens. Upregulation of HO-1 in the substantia nigra of PD subjects supports the view that the affected tissue is experiencing chronic oxidative stress. In addition, excessive cellular levels of heme-derived free iron and carbon monoxide resulting from HO-1 overactivity may contribute to the pathogenesis of PD.
血红素加氧酶-1是一种细胞应激蛋白,在大脑和其他组织中表达,以应对氧化应激和其他有害刺激。在本研究中,采用免疫组织化学方法评估了来自帕金森病(PD)患者和对照受试者的各种死后人类脑标本中HO-1的表达情况。在PD标本和对照标本的黑质中,始终在含神经黑色素的(多巴胺能)神经元中观察到中度HO-1免疫反应性。PD黑质神经元中的路易小体在其周边显示出强烈的HO-1免疫染色。在PD标本和对照标本中,在所调查的其他脑区,神经元HO-1染色微弱或无法检测到。PD黑质中表达HO-1的GFAP阳性星形胶质细胞比例(77.1±12.3)显著高于对照受试者黑质中的比例(18.7±7.1;P = 0.0015)。在其他检查区域,共表达HO-1的GFAP阳性星形胶质细胞百分比相对较低,对照标本和PD标本之间无显著差异(P>0.05)。PD患者黑质中HO-1的上调支持了受影响组织正在经历慢性氧化应激的观点。此外,HO-1过度活性导致的血红素衍生的游离铁和一氧化碳细胞水平过高可能有助于PD的发病机制。