摘要目的 通过bel-2/bax蛋白调控脑白质少突胶质细胞凋亡,研究海洛因海绵状白质脑病(HSLE)的发病机制.方法 病例组4例HSLE及对照组5例非脑部病变4%多聚甲醛溶液固定尸检脑.于大脑额叶、小脑及胼胝体取材,石蜡包埋、切片.进行HE染色,碱性髓鞘蛋白(MBP)、细胞凋亡蛋白酶半胱氨酸蛋白水解酶(caspase)-3、凋亡抑制基因bcl-2及凋亡促进基因bax免疫组化染色.利用显微图像分析观察脱髓鞘的改变并进行灰度分级.计数caspase-3、bel-2、bax阳性点数,作统计学分析.结果 HSLE组小脑、胼胝体、额叶白质均存在髓鞘脱失,以小脑最为明显,灰度级分别为:a、b、c;小脑、胼胝体、额叶白质均有caspase-3表达,均明显高于对照组(P＜0.05);bax阳性表达较对照组高(P＜0.05);bel-2表达与对照组比较,差异无统计学意义(P＞0.05).结论 HSLE病变区存在广泛脱髓鞘改变,bcl-2/bax比值下降所致的少突胶质细胞凋亡可能是发病原因之一.

abstractsObjective To investigate the role of oligodendrocyte apoptosis under the regulafion of the bcl-2/bax protein expression in brain white matter in the pathogenesis of heroin-induced spongiform leucoencephalopathy (HSLE).Methods Samples of frontal lobe,cerebellum,and corpus callosum were obtained from the brains during autopsy of 4 HSLE cases and 5 normal controls and underwent light microscopy and electron microscopy. Immunocytochemistry was used to detect the expression of myelin basic protein(MBP),caspase-3,bel-2 protein,and bax protein.Results Widespread demyelination was seen in the white matter of the frontal lobe,cerebellum and corpus callosum of the HSLE cases,most severely in the cerebellum.The levels of caspase-3 and bax expression of the HSLE group were significantly higher than those of the control group(both P＜0.05),however,the bcl-2 level of the HSLE group was no significantly different from that of the control group(P＞0.05).Conclusion Widespread demyelinafion in the white matter is a prevailed pathological change of HSLE.Oligodendrocyte apoptosis under induced by the decrease of bel-2/bax ratio may contribute to the pathogenesis.