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目的 :探讨增殖性玻璃体视网膜疾病细胞凋亡的信号传导途径 ,以寻求新的药物治疗途径。方法 :2 3例增殖性玻璃体视网膜病变 (PVR) ,增殖性糖尿病性视网膜病变 (PDR) ,黄斑裂孔 (MH)及黄斑前膜 (MP)的视网膜前膜 (epiretinalmem brane,ERM )由玻璃体切割术中取得。细胞凋亡的情况由terminaldeoxynucleotidyltransfrase dUTP nickendlabeling(TUNEL法 )进行评估。Caspase 3及PARP的表达由特异性抗体抗活性Caspase 3和抗P 85片段的PARP检测。Cytokeratin与抗活性的Caspase 3双染色法进行凋亡细胞类型的鉴别。结果 :大多数发生凋亡的细胞为RPE细胞 ,而凋亡细胞与抗活性Caspase 3和抗P 85片段的PARP表达增加相关。细胞凋亡的数目与发生慢性视网膜脱离 (>2个月 )的病例有关 ,但凋亡系数 (apopto sisindex ,AI)在两组间无显著性差异 (1 4 4 2 9vs 3 2 2 86 ,P =0 1877)。PVR ,PDR ,MP各组的凋亡系数分别为 2 32 5 % ,3 4 2 % ,5 5 % ,P值分别为PPVR&PDR>0 1(0 16 85 ) ,PPDR&MP>0 1(0 5 380 ) ,PPVR&MP>0 1(0 8333)。结论 :此项研究发现细胞凋亡在PVR、PDR、MH及MP发病中的重要调节作用。诱导Caspase 3活性表达可作为一种治疗增殖性视网膜疾病的新的尝试
Objective: To investigate the signal transduction pathways of apoptosis in proliferative vitreoretinal diseases in order to seek for new drug treatment approaches. Methods: Two cases of proliferative vitreoretinopathy (PVR), proliferative diabetic retinopathy (PDR), macular hole (MH), and epiretinalmem brane (ERM) of the anterior segment of the macula were treated by vitrectomy Made in. Apoptosis was assessed by terminal deoxynucleotidyltransfrase dUTP nickendlabeling (TUNEL method). The expression of Caspase 3 and PARP was detected by PARP specific anti-active Caspase 3 and anti-P 85 fragments. Identification of apoptotic cell types by Cytokeratin and anti-active Caspase 3 double staining. RESULTS: Most apoptotic cells were RPE cells, while apoptotic cells were associated with increased PARP expression in the anti-active Caspase 3 and anti-P 85 fragments. The number of apoptotic cells was related to the occurrence of chronic retinal detachment (> 2 months), but there was no significant difference in apoptotic index (apoptoisis index, AI) between the two groups (1442-9vs3262, P = 0 1877). The apoptotic index of PVR, PDR and MP groups were respectively 2 32 5%, 34 2% and 55%, P values were PPVR & PDR> 0 1 (0 16 85), PPDR & MP 0 1 (0 5 380) , PPVR & MP> 0 1 (0 8333). Conclusion: This study found that apoptosis plays an important regulatory role in the pathogenesis of PVR, PDR, MH and MP. Induction of caspase 3 activity may serve as a new attempt to treat proliferative retinal diseases