Orihara Yoshiyuki, Tsuda Ryouichi, Ikematsu Kazuya, Nakasono Ichiro, Ogata Mamoru
Department of Legal Medicine, Faculty of Medicine, Kagoshima University, Sakuragaoka 8-35-1, Kagoshima City 890-8520, Japan.
Leg Med (Tokyo). 2003 Mar;5 Suppl 1:S278-9. doi: 10.1016/s1344-6223(02)00149-9.
We investigated the dynamics of the induction of heme oxygenase-1 (HO-1) in the human brain after death caused by traumatic brain injury (TBI). HO-1 was found to stain neurons and microglia/macrophages in cases with TBI, whereas no positive staining except for a few round cells in the arachnoidal space was observed in control cases. In a case with 7h survival, a considerable number of HO-1 positive neurons and microglia were observed. The number of HO-1 positive cells and level of HO-1 staining gradually increased up to 24h survival. Although HO-1 positive neurons were seldom observed in cases with more than 7-day survival, HO-1 positive microglia were still observed even in cases with 5-month survival. The results indicate that HO-1 may be induced by TBI in human cases, and suggest that prolonged HO-1 induction in microglia might reflect its role in protecting those cells from secondary damage including oxidative stress.
我们研究了创伤性脑损伤（TBI）导致的人类死亡后脑组织中血红素加氧酶-1（HO-1）的诱导动力学。在TBI病例中，发现HO-1可对神经元以及小胶质细胞/巨噬细胞进行染色，而在对照病例中，除蛛网膜下腔有少数圆形细胞外未观察到阳性染色。在存活7小时的病例中，观察到相当数量的HO-1阳性神经元和小胶质细胞。HO-1阳性细胞数量和HO-1染色水平在存活至24小时时逐渐增加。尽管在存活超过7天的病例中很少观察到HO-1阳性神经元，但即使在存活5个月的病例中仍可观察到HO-1阳性小胶质细胞。结果表明，HO-1可能在人类TBI病例中被诱导，提示小胶质细胞中HO-1的长时间诱导可能反映了其在保护这些细胞免受包括氧化应激在内的继发性损伤中的作用。
