Effect of PI3K/AKT inhibitor on benign prostate hyperplasia and its mechanism: an experimental study / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the effect of the phosphoinositide 3-kinase/protein kinase B (PI3K/PKB or PI3K/AKT) signaling pathway inhibitor on benign prostate hyperplasia (BPH) and its mechanism.</p><p><b>METHODS</b>Forty-eight SD male adult rats aged 12 weeks were equally randomized to 4 groups: sham operation control, BPH model, 50 mg LY294002 and 100 mg LY294002. The BPH models were made by muscular injection of testosterone propionate at 10 mg/kg/d for 30 days following castration. The LY294002 groups were treated with the PI3K/AKT signaling pathway inhibitor LY294002 at 50 and 100 mg/kg every other day for 30 days. The prostates of the rats were weighed and the structural changes of the prostatic histiocytes observed under the light microscope. The expressions of Ki-67, anti-apoptotic Bcl-2 and apoptotic Bax were detected by immunohistochemistry, and the apoptosis of prostatic cells determined by terminal de-oxynucleotidyl transferase-mediated dUTP nick end labeling.</p><p><b>RESULTS</b>The prostate wet weight and prostatic index were (551 +/- 10.8) mg and 1.61 +/- 0.05 in the sham operation group, (687 +/- 13.8) mg and 2.15 +/- 0.12 in the BPH model group, (623 +/- 23.5) mg and 1.95 +/- 0.11 in the LY294002 50 mg group (P < 0.05 versus the BPH models) and (561 +/- 12.6) mg and 1.71 +/- 0.18 in the LY294002 100 mg group (P < 0.01 versus the BPH models). The expressions of apoptotic Bax and anti-apoptotic Bcl-2 were 16.7% and 16.7% in the sham operation group, 16.7% and 58.3% in the BPH model group, 33.3% and 33.3% in the LY294002 50 mg group (P < 0.05 versus the BPH models), and 50.0% and 25.0% in the LY294002 100 mg group (P < 0.01 versus the BPH models). The proliferative and apoptotic indexes were 14.2 +/- 6.4 and 6.5 +/- 1.8 in the epithelial and 7.6 +/- 2.6 and 2.5 +/- 0.3 in the interstitial tissue of the sham operation group, 50.9 +/- 12.8 and 2.7 +/- 1.4 in the epithelial and 16.5 +/- 5.7 and 1.3 +/- 0.8 in the interstitial tissue of the BPH models, 32.0 +/- 13.8 and 6.2 +/- 2.5 in the epithelial and 12.1 +/- 3.8 and 1.6 +/- 1.1 in the interstitial tissue of the LY294002 50 mg group (P < 0.05 versus the BPH models), and 17.8 +/- 14.7 and 7.4 +/- 3.6 in the epithelial and 9.5 +/- 3.4 and 2.2 +/- 1.3 in the interstitial tissue of the LY294002 100 mg group (P < 0.01 versus the BPH models).</p><p><b>CONCLUSION</b>The increased proliferation and decreased apoptosis of prostatic cells in the BPH animal models might be involved in the development and progression of BPH. The PI3K/AKT signaling pathway plays an important role in the development of BPH, which could be inhibited by blocking the PI3K/AKT signaling pathway.</p>

Cytogenetic analysis and phenotype location analysis on the karyotype of a ring chromosome 21 syndrome / 中华医学遗传学杂志

<p><b>OBJECTIVE</b>To search the forming cause and the correlation between the clinical phenotype and chromosome band by the cytogenetic analysis on a case of ring chromosome 21 syndrome.</p><p><b>METHODS</b>Identification and location of 21 ring chromosome were performed with the G-banding, C-banding, N-banding, high-resolution banding and fluorescence in situ hybridization (FISH) techniques.</p><p><b>RESULTS</b>It was found that the karyotypes of the patient's parents are normal. The patient's karyotype is 46,XY, r(21)[91]/46,XY,r(21;21)(p11q22.3;p11q22.3) [5]/45,XY,-21[4].</p><p><b>CONCLUSION</b>The clinical phenotype of ring chromosome 21 syndrome is related to the deletion of distal segment of 21q, and the abnormal sexual development of male is related with the deletion of 21q22.3.</p>