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首页> 外文期刊>Research Journal of Biological Sciences >3A Study of the Significance of Apoptosis and its Association with Abnormalities in Expression of BCL-2 Proto-Oncogene in Benign Nodular Hyperplasia of Prostate
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3A Study of the Significance of Apoptosis and its Association with Abnormalities in Expression of BCL-2 Proto-Oncogene in Benign Nodular Hyperplasia of Prostate

机译:3A前列腺良性结节性增生中细胞凋亡的意义及其与BCL-2原癌基因表达异常的关系

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Benign Prostatic Hyperplasia (BPH) is an enlargement of the prostate gland caused by an increase in the number of glandular units. Apoptosis is a programmed cell death necessary for the regulation of the size of organs in adult life. Disruption of apoptotic pathways has been suggested as an important regulatory mechanism in BPH. A high level of the BCL-2 protein suppresses apoptosis by preventing the activation of the enzymes that carry out the process. In this study, an attempt was made to observe the abnormal expression of BCL-2 protein in BPH tissues in paraffin sections and to demonstrate the disruption of apoptotic pathways in BPH. Prostatic tissue from 30 patients with BPH and no prior prostatic carcinoma were obtained by transurethral resection of prostate procedure. Apoptotic index was compared in the H and E sections. Expression of BCL-2 was analyzed by immunohistochemistry and evaluated. Apoptotic index in BPH tissues was found to be twice lower than that of normal tissues. Wilcoxon signed rank test was employed and the p-value proved that the results were highly significant (p<0.01). This data supported the research hypothesis that apoptotic index is decreased in benign prostatic hyperplasia. Out of 30 tissue samples, 20 (67%) shown positivity for BCL-2 expression. Kendall’s Tau-B test was applied and the result showed negative correlation between the intensity of BCL-2 expression and apoptosis, however not significantly. This proves, the theory that BCL-2 regulates individual cell death up to a certain extent.
机译:良性前列腺增生(BPH)是由于腺单位数量增加而引起的前列腺增大。凋亡是调节成年生活中器官大小所必需的程序性细胞死亡。凋亡途径的破坏已被认为是BPH中的重要调节机制。高水平的BCL-2蛋白可通过阻止执行该过程的酶的激活来抑制细胞凋亡。在这项研究中,试图观察石蜡切片中BPH组织中BCL-2蛋白的异常表达,并证明BPH中凋亡途径的破坏。经尿道前列腺前列腺切除术从30例BPH且无既往前列腺癌的患者中提取前列腺组织。在H和E部分比较细胞凋亡指数。通过免疫组织化学分析并评估BCL-2的表达。发现BPH组织中的细胞凋亡指数比正常组织低两倍。采用Wilcoxon符号秩检验,p值证明结果非常显着(p <0.01)。该数据支持了在良性前列腺增生中凋亡指数降低的研究假设。在30个组织样本中,有20个(67%)显示出BCL-2表达的阳性。进行了Kendall的Tau-B测试,结果显示BCL-2表达强度与细胞凋亡之间呈负相关,但无明显关系。这证明了BCL-2在一定程度上调节单个细胞死亡的理论。

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