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目的:研究爱普列特是否通过诱导前列腺细胞凋亡来治疗前列腺良性增生。探讨以前列腺酸性磷酸酶作为前列腺萎缩标志的可行性。方法:光镜观察细胞形态变化。TUNEL法和琼脂糖凝胶电泳检测DNA断裂。测定前列腺酸性磷酸酶的活性。结果:去势和爱普列特均诱发前列腺细胞发生细胞凋亡。去势引发的细胞凋亡的程度大于爱普列特。爱普列特和去势均降低了前列腺湿重和DNA含量,升高了DNA浓度。最大或接近最大的抑制发生在给药后10天。爱普列特抑制了前列腺酸性磷酸酶的活性,其变化与给药或去势后前列腺湿重和DNA含量的变化一致。结论:爱普列特通过诱发前列腺细胞凋亡来治疗前列腺良性增生。前列腺酸性磷酸酶的活性可作为前列腺萎缩的标志。
Aims: To study whether epristeride is involved in benign prostatic hyperplasia by inducing apoptosis of prostatic cells. To explore the feasibility of prostatic acid phosphatase as a marker of prostatic atrophy. Methods: The morphological changes of cells were observed by light microscope. DNA fragmentation was detected by TUNEL and agarose gel electrophoresis. Prostate acid phosphatase activity was measured. Results: Both castration and eprostine induce apoptosis of prostatic cells. Castration induced apoptosis more than eprotectic. Epristeride and castration both reduce prostate wet weight and DNA content, increasing DNA concentration. The maximal or near maximal inhibition occurs 10 days after dosing. Epsilon inhibits prostatic acid phosphatase activity, which is consistent with changes in prostatic wet weight and DNA content after administration or by castration. Conclusion: Epristeride treatment of benign prostatic hyperplasia by inducing apoptosis of prostate cells. Prostate acid phosphatase activity can be used as a sign of prostate atrophy.