补骨脂素抗良性前列腺增生的研究

目的探讨补骨脂素对丙酸睾丸酮所致大白鼠前列腺增生(BPH)模型的作用。方法将SD大鼠去势7 d后皮下注射丙酸睾丸酮5.00 mg·kg-1·d-1,同时以补骨脂素45.00、15.00mg·kg-1·d-1保列治0.45 mg·kg-1·d-1、蒸馏水0.10 ml·kg-1·d-1,灌胃治疗1个月后处死大鼠,称量前列腺湿重、体积,光镜观察前列腺组织病理学改变、放射免疫法测量血清睾酮(T)和雌二醇(E2)。结果 补骨脂素组的前列腺湿重指数[(6 723.1±763.3、6 434.8±481.3)mg/kg体重]和前列腺体积指数[(3.8±0.7、4.4±0.8)ml/kg体重]较保列治组[(6 820.8±528.2)mg/kg体重、(5.4±0.3)ml/kg体重]及蒸馏水组[(8 798.5±1 184.9)mg/kg体重、(6.7±1.1)ml/kg体重]显著降低(P<0.05)。补骨脂素组前列腺组织增生程度较保列治组及蒸馏水组显著降低(P<0.05);补骨脂素对丙酸睾丸酮所致前列腺增生模型大白鼠的血清T和E2的表达差异无显著性(P>0.05)。结论补骨脂素治疗丙酸睾丸酮所致大鼠前列腺增生有效。     

维生素D对前列腺增生小鼠血清生化指标的影响研究

目的 通过观察维生素D对前列腺增生小鼠动物模型血清生化指标的影响,探讨不同剂量维生素D对前列腺增生动物模型的血清生化指标影响.方法 应用丙酸睾酮肌肉注射制造小鼠前列腺增生模型.随机分组,采用不同剂量的维生素D剂喂养4周后,检测小鼠血清电解质、肝肾功能、血脂等指标.结果 应用0.2、1.0和5.0 μg/kg·d~(-1)的各组小鼠检测结果显示:应用维生素D对前列腺增生小鼠的肾功能无明显负面影响;但是大剂量维生素D对血清谷草转氨酶(AST)有升高作用;中、大剂量维生素D可以升高血清钙离子浓度,对镁、磷无明显影响.结论 中、小剂量维生素D对小鼠前列腺增生模型的肝肾功能、电解质未发现明显负面影响,大剂量维生素D可能对血清钙离子浓度、AST有一定影响.     

前列舒通对丙酸睾酮诱导的去势大鼠前列腺增生的作用机制

目的探讨前列舒通抑制良性前列腺增生的治疗作用机理,观察其对良性前列腺增生的治疗效果。方法观察前列舒通作用于丙酸睾酮诱导去势大鼠前列腺增生模型后的前列腺指数,前列腺体积,前列腺腺体总面积、bFGF(碱性成纤维生长因子)、EGF(表皮生长因子)、bcl-2(抑制细胞凋亡因子),以及前列腺组织病理学改变。结果前列舒通各浓度组前列腺指数、前列腺体积、前列腺腺体总面积、bFGF、EGF、bcl-2均明显低于模型组。结论前列舒通能显著抑制丙酸睾酮诱导去势大鼠的良性前列腺增生,其机制可能是通过降低bFGF、EGF、bcl-2的表达水平,从而抑制前列腺细胞增殖和促进凋亡而实现的。     

中医不同治法对骨质疏松症小鼠骨密度、碱性磷酸酶、抗酒石酸酸性磷酸酶影响的实验研究

目的 观察中医不同治法对骨质疏松症小鼠骨密度（BMD)、碱性磷酸酶(ALP)、抗酒石酸酸性磷酸酶(TRAP)变化的影响，探讨中医防治骨质疏松症的机制。方法 除正常组外，将骨保护素（OPG)基因敲除小鼠随机分为模型组、补肾组、健脾组、活血组和福善美组。检测各组小鼠BMD及血清ALP、TRAP含量。结果 1.与正常组比较，模型组小鼠BMD显著降低(P <0. 05)；与模型组比较，补肾组与健脾组BMD显著升高(P < 0. 05)。2.与正常组比较，模型组小鼠血清ALP含量显著升高(P <0.05);与模型组比较，补肾组、健脾组和福善美组小鼠血清ALP含量显著降低(P <0.05)。3.与正常组比较，模型组小鼠血清TRAP含量显著升高(P <0.05);与模型组比较，补肾组与健脾组小鼠血清TRAP含量显著降低(P <0.05)。结论补肾和健脾方法能显著提高骨质疏松小鼠的骨量，明显抑制成破骨活性，使小鼠脱离高骨转换状态，起到治疗骨质疏松症的作用。     

桂枝不同提取物对大鼠良性前列腺增生的影响

目的:观察桂枝不同提取物对丙酸睾丸素致大鼠良性前列腺增生的影响。方法:皮下注射丙酸睾丸素(雄性大鼠5mg/kg)造成良性前列腺增生动物模型。给药组分别灌胃给予桂枝不同成分提取物,前列康组相同途径给予前列康混悬液(雄性大鼠2.0g/kg),正常对照组和模型组给以等体积离子净化水。给药期间收集尿液。末次给药24h后取前列腺,计算前列腺指数并进行病理学切片检查。结果:桂枝水煎液具有一定的利尿作用,可明显降低良性前列腺增生模型大鼠的前列腺湿重和前列腺指数(P<0.01),光镜下可观察到其能明显改善前列腺组织病理现象。结论:桂枝水煎液有治疗大鼠良性前列腺增生作用。     

消癃通闭对小鼠前列腺上皮细胞DNA合成的影响

去势昆明雄性小鼠24只,皮下注的丙酸睾丸素5mg/kg·d~(-1),同时将其分为4组,分别给予高剂量消癃通闭、低剂量消癃通闭、雌二醇及睾丸素。于15天、30天时分别腹腔注射~3H TdR(20uci/g),24小时后处死,取前列腺右头叶和腹叶称重,制成石腊切片进行放射自显影,观察前列腺上皮细胞核上标记银盐颗粒。结果结示~3H TdR标记呈不均一性,腺管末梢标记明显。单纯给予丙酸睾丸素组被标记的腺上皮明显高于其它组。用消癃通闭15天后标记细胞减少,但30天后4组间无明显差异。提示消癃通闭对小鼠前列腺的生长、DNA合成有抑制作用。前列腺内DNA合成局限于腺管末梢,前列腺发育到一定程度,其合成也相对停止。     

耻骨上前列腺增生切除术的偶发癌

耻骨上前列腺增生切除术的偶发癌沈思从１９８６年５月～１９９６年１０月行耻骨上前列腺切除术２９２例，发现前列腺偶发癌１３例，报告如下。资料与方法本组临床诊断为前列腺增生症２９２例，年龄５９～７８岁，平均６５．９岁。经体查，Ｂ超前列腺检查，血清酸性磷酸酶...     

他莫昔酚对大鼠前列腺增生动物模型的抑制作用及机理研究

目的 :探讨他莫昔酚抑制前列腺增生的作用机理。　方法 :将Wistar成年大鼠肌肉注射丙酸睾丸酮 ,同时以他莫昔酚常规灌胃。于给药 7、15、30d时分批处死大鼠 ,称取前列腺重量 ,标本做常规病理切片 ,电镜观察前列腺组织细胞结构变化。　结果 :给药 7d时单用睾酮组前列腺指数高于对照组 ,也高于灌胃组。剩余大鼠分 2组 ,其中 1组继续单用他莫昔酚灌胃 ,于第 15、30d时分组处死剩余大鼠。光镜染色观察及电镜扫描均证实他莫昔酚组前列腺上皮细胞及基质的增殖被抑制。　结论 :他莫昔酚通过对雌激素的拮抗作用 ,阻断雌激素在前列腺增生中的作用 ,从而抑制前列腺增生。     

乳腺康对实验性雌激素水平增高和乳腺组织增生的影响

目的：了解乳腺康对雌激素引起的大白鼠性激素水平增高和乳腺组织增生的影响。方法：１０周龄雌性ＳＤ大鼠隔天注射０．４ｍｇ／ｋｇ体重苯甲酸雌二醇，同时每天灌服三苯氧胺、乳癖消或不同剂量的乳腺康冲剂３０天。结果：注射苯甲酸雌二醇动物体重降低并且引起血清雌激素含量显著增高，经用三苯氧胺或乳癖消治疗无显著疗效，而灌服中剂量和高剂量乳腺康的动物均能显著地降低血清雌激素含量；注射苯甲酸雌二醇能引起大鼠乳房肿大，三苯氧胺能抑制苯甲酸雌二醇引起的乳房肿大，乳癖消作用不明显，而灌服不同剂量的乳腺康冲剂均能不同程度地抑制乳房肿大。结论：乳腺康能治疗雌激素引起的乳腺病，其作用优于三苯氧胺和乳癖消     

滋肾丸对去势骨质疏松雌鼠骨生物力学性能的改善作用及机制的实验研究

目的 探讨补肾中药滋肾丸对去卵巢骨质疏松模型大鼠腰椎的骨生物力学性能的改善作用及机制研究.方法 将66只15周龄SD大鼠随机分为6组,每组11只,空白组做假手术,其余5组做卵巢切除术,术后2周开始给药,用药12周后处死,测定腰1椎体的最大载荷和破坏应力,血清雌二醇、碱性磷酸酶含量.结果 模型大鼠腰1椎体的最大载荷和破坏应力明显下降,血清碱性磷酸酶升高,血清雌二醇下降,滋肾丸大、中剂量组均能对抗上述指标的变化,差异均有统计学意义（P＜0.05）.结论 补肾中药滋肾丸对去卵巢骨质疏松大鼠骨的生物力学性能有明显的改善作用,其机制与其升高血清雌二醇,降低血清碱性磷酸酶含量进而抑制过高的骨转换有关.     

3'-大豆苷元磺酸钠抗实验性小鼠良性前列腺增生的作用观察

目的:研究3'-大豆苷元磺酸钠(DSS)对实验性小鼠BPH及性激素平衡的影响。方法:40只雄性小鼠随机分为5组:正常对照组、BPH模型组、前列康组(阳性对照)、20mg/(kg.d)DSS组及40mg/(kg.d)DSS组,每组8只。皮下注射丙酸睾酮建立小鼠BPH模型。正常对照组给予橄榄油0.1ml/只,前列康组给予前列康5g/(kg.d),DSS组给予DSS20mg、40mg/(kg.d)灌胃。观察每组处理12d后小鼠前列腺湿重、前列腺指数、前列腺组织形态学变化和性激素水平。结果:DSS治疗12d后,与模型组相比,DSS组小鼠前列腺湿重及前列腺指数出现剂量依赖性的降低(P(0.05或P(0.01),光镜下见增生的腺上皮乳头减少或消失,腺体上皮细胞呈低立方或扁平状;血清T、E2含量和T/E2比值明显降低(P(0.05或P(0.01),40mg/(kg.d)DSS组的结果与前列康组相似。结论:DSS对丙酸睾酮所致小鼠BPH具有显著的拮抗作用,其作用机制在一定程度上与降低小鼠血清T、E2含量及T/E2比值有关。     

Serum hormone levels among patients with prostatic carcinoma or benign prostatic hyperplasia and clinic controls

This study sought to identify differences in serum hormone levels between prostatic cancer (CaP) patients, benign prostatic hyperplasia (BPH) patients, and clinic controls (CC). Serum testosterone, estradiol, and prolactin values were obtained from 35 CaP, 42 BPH, and 161 CC patients attending a single medical center between January 1984 and April 1985. Relative risk estimates adjusted for age and race were calculated to compare hormone values between each case group and the CC. The distributions of hormone values and the testosterone to estradiol (T/E) ratios were grouped into thirds with the lowest third forming the reference category. The relative risk estimates for BPH in the middle and high thirds of testosterone were greater than unity (1.26 and 2.10, respectively), whereas the relative risk estimates in the middle and high thirds of estradiol were less than unity (0.63 and 0.35, respectively). For the middle and high thirds of the T/E ratio, the relative risk estimates for BPH showed statistically significant three- to fourfold increases. Modest depression of serum testosterone and estradiol was noted for CaP patients compared to CC, although the differences were not statistically significant. This depression was interpreted to be a likely result of the malignant process rather than a cause of it, whereas the development of clinically evident BPH was felt to be a biologically plausible response to an elevated T/E ratio.     

Effect of hormone treatment on prostatic acid phosphatase in a serially transplantable human prostatic adenocarcinoma (PC-82)

The influence of endocrine manipulation on the tissue concentration of prostatic acid phosphatase (PAP) was studied in the hormone dependent transplantable human prostatic tumor line PC-82. Tumor bearing nude mice were left intact, castrated or treated for a 5-day period with a subcutaneous implant containing testosterone or estradiol. The concentration of PAP in castrated mice was not different from that in the controls. The DNA content of PC-82 tumor tissue obtained from 5-day castrated animals was significantly lower than that of tissue from intact animals. Therefore the concentration of PAP in tissue from castrated mice was significantly elevated when expressed per mg. of DNA (p less than 0.05). Treatment of the mice with testosterone or estradiol did not affect the PAP concentration in the tumor tissue. A significant correlation was observed between the concentration of PAP in the serum and the tumor burden of the mice. Long-term withdrawal of androgens resulted in a decrease of the concentration of PAP in the serum, as well as in a decrease of the tumor burden. The concentration of PAP in the tumor tissue remaining after castration of these animals was not significantly different from that in controls. The present data from the tumor line PC-82 do not support the hypothesis that the concentration of PAP in prostatic tumor tissue is controlled by androgens, but are in agreement with the concept that the level of PAP in plasma is related to the tumor mass.     

Changes in the endocrine environment of the human prostate transition zone with aging: simultaneous quantitative analysis of prostatic sex steroids and comparison with human prostatic histological composition

BACKGROUND: It is well-known that the incidence of benign prostatic hyperplasia (BPH) increases with aging. The age-dependent changes in the ratio of serum sex steroid concentrations may play a role in BPH development. To clarify the relationship between the prostatic tissue concentrations of these steroids and age, we established a precise method of simultaneous quantitative analysis for prostatic sex steroids and used this method to investigate the tissue concentrations of three major sex steroids (testosterone, dihydrotestosterone, and estradiol) in the human prostate. METHODS: The methodology for the simultaneous quantitative analysis of prostatic sex steroids was established using castrated rat prostatic tissue, coupled with internal standards, for androgen-deprived medium, and the validation of the method was examined. Human prostatic tissues were collected during surgery and immediately frozen at -70 degrees C. Using our method, the steroidal fractions were extracted, purified, and quantified. The proportions of stroma, epithelium, and glandular lumen were measured on each histological specimen, using an image analyzer. RESULTS: The validation tests showed that our method of quantitative analysis was precise and sensitive enough for the quantification of testosterone, dihydrotestosterone, and estradiol in the prostate. In humans, the prostatic dihydrotestosterone concentration decreased with age, but the concentrations of testosterone and estradiol showed no relation with age. Therefore, the ratio of estradiol to dihydrotestosterone concentration (E2/DHT) in prostate increased with age. The E2/DHT ratio showed a significant positive correlation with the proportion of stroma. CONCLUSIONS: The age-dependent decrease in prostatic dihydrotestosterone and constant estradiol concentration lead to a relatively estrogen-dominant environment compared to that at younger ages. We assume that this relatively estrogen-dominant status induces stromal proliferation by some mechanism and leads to the development of BPH.     

Impact of polychlorinated biphenyl （Aroclor 1254） and vitamin C on antioxidant system of rat ventral prostate

Aim: To evaluate the effect of polychlorinated biphenyls (PCB) and vitamin C on ventral prostatic antioxidant system in adult male rats. Methods: A group of 20 adult male rats were administered ip Aroclor 1254 in corn oil at a dose of 2 mg·kg-1·day-1 for 30 days. Ten control rats were administered only the vehicle. After 30 days the treated rats were divided at random into 2 sub-groups of 10 animals each. One sub-group received vitamin C at a dose of 500 mg·kg-1·day-1 for 10 days. The other group was maintained as Aroclor 1254 control. Twenty-four hours after the last treatment the rats were killed by decapitation. Ventral prostatic homogenate was prepared and used for the estimation of enzymatic antioxidants, including superoxide dismutase (SOD), catalase (CAT) and glutathione-S-transferase (GST) and hydrogen peroxide (H2O2), lipid peroxidation (LPO) and prostatic acid phosphatase. The serum levels of total T3, total T4, TSH, testosterone and estradiol were also assayed. Results: The body weight and     

Progressive prostate hyperplasia in adult prolactin transgenic mice is not dependent on elevated serum androgen levels

BACKGROUND: Transgenic mice overexpressing the rat prolactin (PRL) gene under control of the metallothionein-1 promoter (Mt-1) develop a dramatic prostatic enlargement. These animals also display significantly elevated testosterone serum levels. In this study, we aim to clarify the role of circulating androgen levels in the promotion of abnormal prostate growth in the adult PRL transgenic mouse prostate. METHODS: Prostate morphology and androgen-receptor distribution patterns were analyzed in castrated and testosterone substituted adult PRL transgenic and in wild-type males. RESULTS: Progressive prostatic hyperplasia in adult PRL transgenic males was not affected by substitution to serum testosterone levels corresponding to wild-type. Furthermore, prolonged testosterone treatment in adult wild-type males did not produce any significant changes in prostate growth or morphology compared with wild-type controls. Immunohistochemical studies revealed a significantly increased proportion of androgen receptor positive epithelial cells in all lobes of the PRL transgenic prostate versus wild-type. CONCLUSION: The present study demonstrates that progressive prostate hyperplasia in adult PRL transgenic mice is not dependent on elevated serum androgen levels. Furthermore, prolonged androgen treatment in adult wild-type male mice appears to have no significant effect on prostate growth. In addition, our results suggest that prolonged hyperprolactinemia results in changes in prostate epithelial and stromal cell androgen receptor distribution.     

Changes in serum acid and alkaline phosphatase and leucine aminopeptidase activities following massage of the prostate

The changes in serum alkaline phosphatase, total acid phosphatase, prostatic acid phosphatase and leucine aminopeptidase activities following massage of the prostate in patients with carcinoma or benign hyperplasia of the prostate having premassage control activities of a definite range were studied. Statistical significance of results was calculated by the F method. The results are as follows: 1) Following massage of the prostate the total serum acid phosphatase activity increased significantly, more markedly in benign hyperplasia than in carcinoma, and this may help to differentiate benign hyperplasia from carcinoma of the prostate. 2) Following massage of the prostate, serum alkaline phosphatase, prostatic acid phosphatase and leucine aminopeptidase activities showed no significant changes in either group.     

The changes in the binding capacity of testosterone-oestradiol binding globulin (TeBG) following castration and DES-D administration in patients with prostatic carcinoma

Summary The levels of plasma testosterone, testosterone-oestradiol binding globulin (TeBG) and total serum acid phosphatase (TSAP) following antiandrogenic hormone therapy were investigated in 17 patients with prostatic carcinoma. The low levels of plasma total and free testosterone induced by castration decreased further after diethylsitlboestrol diphosphate (DES-D) administration. Plasma TeBG binding capacity after castration was 118.9% of the pre-treatment level and increased to 193.9%, 204.0% and 212.7% at 1, 2 and 3 weeks after DES-D dosing. The in vitro binding of ³H-testosterone to TeBG was not influenced in the presence of DES-D or stilboestrol. Clinical response following the DES-D therapy was associated with a decrease in the levels of TSAP. A significantly inversed correlation was found between the decrease in TSAP and increase in TeBG at completion of DES-D therapy. These results suggest that the high binding capacity of TeBG lowers the biologically active fraction of testosterone and thus may produce clinical effects.     

Circadian and day-to-day variation of prostatic acid phosphatase

The circadian and day-to-day variation of serum levels of prostatic acid phosphatase determined by radioimmunoassay was investigated in 10 men with a normal prostate, 8 with benign prostatic hyperplasia and 10 with prostate cancer. Serum samples were obtained on 1 day at 8 a.m., 12:00 noon and 4:30 pm. in 23 patients, and on 3 consecutive days at 8 a.m. in an additional 5 patients. There was a variability in enzyme level throughout the day but without any distinct pattern. Prostate cancer patients with elevated levels of prostatic acid phosphatase did demonstrate a greater variability throughout the day than patients with a normal prostate or with benign prostatic hyperplasia. The day-to-day serum prostatic acid phosphatase in patients with a normal prostate varied little and remained within the normal range.     

Testosterone-induced decrement of prostatic vascular resistance in rats is reversed by estrogens

The function and growth of the rat prostate are stimulated by androgens and inhibited by estrogens. To study the influence of these hormones on the prostatic blood flow, prostatic vascular resistance was measured in castrated adult rats, which were testosterone supplemented and treated with different estrogenic substances. Prostatic blood flow was measured using the microsphere technique. Testosterone supplementation for 8-9 days after castration resulted in decreased vascular resistance in both the ventral and dorsolateral prostates. In testosterone-supplemented rats, treatment for the same period of time with estradiol benzoate, ethinyl estradiol, and diethylstilbestrol induced increased vascular resistance in both the ventral and dorsolateral prostates. However, treatment with estromustine or estramustine did not change prostatic vascular resistance significantly. It was concluded that the testosterone-induced decrease of prostatic vascular resistance was reversed by estradiol, ethinyl estradiol, and diethylstilbestrol, possibly by a direct effect on the prostate.