摘要
目的:探讨凋亡基因Fas和FasL与慢性缺氧肺动脉高压(pulmonary hypertension,PH)心肌细胞凋亡的关系。 方法:23例慢性严重肺源性疾病缺氧新生儿分为两组,缺氧无肺动脉高压组(n=8),缺氧并肺动脉高压组(n=15);正常对照组6例,均为尸检时留取少许左室心肌组织,利用免疫组化及原位杂交技术,对Fas和FasL进行半定量分析。 结果:免疫组化染色用性反应为心肌细胞胞浆均呈棕黄色片状颗粒,原位杂交阳性信号为胞浆及胞膜内为紫蓝色颗粒,而两种染色在对照组心肌细胞胞浆内均未见阳性反应。缺氧及缺氧性PH患儿左室心肌组织 Fas与FasL的mRNA水平及其蛋白质含量均明显升高,与正常对照组比较,差异均有显著性意义(t=17.17～43.01,P均<0.01),而缺氧PH组与缺氧无PH组患儿左室心肌组织Fas与FasL的mRNA水平及其蛋白质含量差异无显著性意义(t=0.30～1.16,P均>0.05)。 结论:Fas系统是参与介导缺氧心肌细胞凋亡的重要环节,而肺动脉高压没有使其表达进一步上调。
AIM: To explore the relation of Fas and FasL with cardiac myocyte apoptosis in neonates with hypoxia-induced pulmonary hypertension (PH). METHODS: A total of 23 neonates with chronic severe hypoxia-induced pulmonary diseases were divided into 2 groups: neonates with hypoxia-induced PH group(n = 15) and 8 without PH, another 6 normal neonates were involved as the control group. The expression of Fas and FasL were investigated by immunohistochemical analysis and in situ hybridization assays in the left ventricular myocardial tissues removed at necropsy. RESULTS: Buffy sheet-shape granules were found in plasm of cardiomy-ocytes by immunohistochemical staining, and royal blue granules were found both inter-and intra-membrane of cardiomyocytes by in situ hybridization. In both in situ hybridization and immunohistochemical studies, neither expression described above was found in the control group. Immunohistochemical analysis and in situ hybridization assays revealed mRNA and protein expression of Fas and FasL were increased significantly in the PH and non-PH, compared with those in the normal control group( t = 17. 17 - 43. 01, P < 0. 01), but there were no significant differences between the PH and non-PH groups( t =0.30-1. 16, P > 0.05).
CONCLUSION: Fas system plays an important role in mediating chronic hypoxia-induced myocyte apoptosis, and it hasn't up-regulated by pulmonary hypertension.
出处
《中国临床康复》
CSCD
2004年第9期1728-1729,F003,共3页
Chinese Journal of Clinical Rehabilitation
