BACKGROUND: To determine the mechanism by which prostate volume increases during the development of BPH and to evaluate the effect of LSESr (Permixon), a phytotherapeutic agent, we investigated apoptosis and cell proliferation in the stroma and epithelium of normal prostate and of BPH tissues from patients treated with or without LSESr. METHODS: MIB-1 staining and the in situ end-labeling assay were used to evaluate the proliferative-apoptotic balance in normal prostates and in BPH tissues. Quantitative assessment was performed using an image analysis system. RESULTS: In normal prostates, there was no significant difference between apoptotic and proliferative indices. Cell numbers and proliferative indices were higher in BPH than in normal prostates, while apoptosis values were similar. In the BPH treated group, LSESr significantly inhibited proliferation and induced cell death in both epithelium and stroma. CONCLUSIONS: Induction of apoptosis and inhibition of cell proliferation are likely to be the basis for the clinical efficacy of LSESr. Copyright 2000 Wiley-Liss, Inc.
BACKGROUND: To determine the mechanism by which prostate volume increases during the development of BPH and to evaluate the effect of LSESr (Permixon), a phytotherapeutic agent, we investigated apoptosis and cell proliferation in the stroma and epithelium of normal prostate and of BPH tissues from patients treated with or without LSESr. METHODS: MIB-1 staining and the in situ end-labeling assay were used to evaluate the proliferative-apoptotic balance in normal prostates and in BPH tissues. Quantitative assessment was performed using an image analysis system. RESULTS: In normal prostates, there was no significant difference between apoptotic and proliferative indices. Cell numbers and proliferative indices were higher in BPH than in normal prostates, while apoptosis values were similar. In the BPH treated group, LSESr significantly inhibited proliferation and induced cell death in both epithelium and stroma. CONCLUSIONS: Induction of apoptosis and inhibition of cell proliferation are likely to be the basis for the clinical efficacy of LSESr. Copyright 2000 Wiley-Liss, Inc.