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以前列腺增生老龄犬,经口服给消癃通闭药粉2g/kg/天及1g/kg/天,连续32天后放血处死。开腹取前列腺组织液氮冻存。RIA测定前列腺组织中T(睾酮)、DHT(双氢睾酮)、E_2(雌二醇);并与血清中浓度对照。Scatchard Plots方法及双复管单点法测定Androgen Receptor Assay(AR)(雄激素受体);酶学法测定5α—还原酶(Ⅰ、Ⅱ型)。结果表明:消癃通闭可抑制胞浆及胞核中5α—还原酶活性,并发现正常犬微粒体中5α—还原酶Ⅰ型酶活性为97.145±52.829,Ⅱ型酶活性为15.745±15.093DHT.Pmol/mg Protein/30min。前列腺增生犬分别为183.152±128.119,69.099±43.391DHT/mg Protcin/30min;消癃通闭1g/kg/天组犬测定值分别为92.454±52.703,11.328±12.06;2g/kg/天组测定值分别为42.837±36.909,9.288±13.209。前列腺组织中AR各组测定值无明显差异。同时发现,前列腺组织中T及DHT值明显高于血清中测定值。用药前后,犬前列腺组织中及血清中E_2、T、DHT值无明显变化。结果表明:消癃通闭治疗前列腺增生的机理为抑制前列腺组织中5α—还原酶的活性。
Old dogs with benign prostatic hyperplasia were orally given 2 g/kg/day and 1 g/kg/day of oral elimination powder and were sacrificed after 32 consecutive days of bleeding. Open abdominal tissue to take liquid nitrogen cryopreservation. The RIA measured T (testosterone), DHT (dihydrotestosterone), and E 2 (estradiol) in prostate tissue and was compared with serum concentrations. Scatchard Plots method and double-tube single-point method for the determination of Androgen Receptor Assay (AR) (androgen receptor); enzymatic determination of 5α-reductase (type I, II). The results showed that the activity of 5α-reductase in the cytoplasm and nucleus was inhibited by the elimination of pupa, and the activity of 5α-reductase type I in normal microsomes was 97.145±52.829, and that in type II was 15.745±15.093DHT. .Pmol/mg Protein/30min. The dogs with benign prostatic hyperplasia were 183.152±128.119,69.099±43.391 DHT/mg Protcin/30min, respectively. The values measured in the canine closed 1g/kg/day dogs were 92.454±52.703 and 11.328±12.06, respectively; 2g/kg/day were measured. They were 42.837±36.909, 9.288±13.209, respectively. There was no significant difference in the measured values of AR in prostate tissue. At the same time, it was found that the T and DHT values in prostate tissue were significantly higher than those in serum. Before and after administration, there was no significant change in the E2, T, and DHT values in the prostate tissue and serum of dogs. The results showed that the mechanism of the treatment of benign prostatic hyperplasia by the elimination of phlegm and blood stasis was to inhibit the activity of 5α-reductase in prostate tissue.