中药阳起石温肾作用实验研究

目的 通过动物实验研究阳起石的温肾功效.方法 以氢化可的松肌肉注射小鼠造成阳虚动物模型,选用以透闪石为基源的阳起石商品药材进行试验.结果 阳起石可明显改善阳虚小鼠外观、增加活动频数、延长低温游泳时间、增强红细胞免疫功能.结论 以透闪石为基源的阳起石药材具有温肾作用.且基本上呈量效关系.     

龙丹丸的壮阳药理作用和急性毒性

龙丹丸为中药复方制剂。龙丹丸灌胃给药,对雄性小鼠具有增加交尾作用(2.0,4.0g/kg),龙丹丸2.0g/kg组的交尾作用明显强于海马多鞭九4.0g/kg组;对幼鼠具有促雄性激素作用(1.0、2.0、4.0g/kg),龙丹丸大、中、小3个剂量组小鼠体重和包皮腺重量明显高于雄狮丸组,龙丹丸大剂量组睾丸重量明显高于雄狮丸组,龙丹丸大、中、小3个剂量组包皮腺重量明显高于海马多鞭丸组;对去势小鼠具有雄激素样作用,这种作用与雄狮丸相似,而海马多鞭丸没有这种作用。灌胃给予龙丹丸80.0g/kg,小鼠未发生死亡,腹腔给予龙丹丸0.5,1.0g/kg,仅1.0g/kg组10只小鼠中死亡1只。     

葱白汁对小鼠壮阳的药理实验报告

用葱白汁ｉｇ给药，以三宝双喜为阳性对照组进行小鼠壮阳药理实验。结果表明，葱白汁和三宝双喜均有增力口雄性小鼠交尾、雄性激素（血浆睾酮）含量以及包皮腺、前列腺精囊重量的作用。     

复方蚂蚁酒对小鼠附性器官及血清睾酮和一氧化氮的影响

目的 探讨复方蚂蚁酒对小鼠附性器官质量及血清睾酮和一氧化氮含量的影响.方法复方蚂蚁酒按生药1.2 g.kg^-1和4.8 g.kg^-1剂量给小鼠灌胃,观察幼年去势小鼠、青年小鼠和老年小鼠附性器官质量,测定青年小鼠精子数,检测老年小鼠血清睾酮和一氧化氮(NO)含量.结果复方蚂蚁酒能明显增加幼年去势小鼠精液囊 前列腺和包皮腺质量,提高青年小鼠的睾丸质量和精子数,增加老年小鼠睾丸质量,提高老年小鼠血清睾酮和NO含量.结论复方蚂蚁酒能增加小鼠附性器官质量,其机制可能与其提高小鼠血清睾酮和NO含量有关.     

太和春胶囊药理及毒理学研究

以太和春水煎剂按１．２，０．６ｇ生药／ｋｇ，进行药产学观察。结果表明能使小鼠体内精子数增加，延长精子存活时间，提高小鼠性欲功能，使小鼠及去势小鼠性腺增重，血清睾酮含量增加，对氢化可的松所致“虚证”的胸腺。脾脏有增重作用。提示本品具有雄激素样作用。毒理实验表明：小鼠ｐｏＬＤ５０＞２０ｇ／ｋｇ，相当于成人一日量的３３３倍。     

三子强肾混悬颗粒补肾壮阳及抗疲劳作用的研究

目的：考察三子强肾混悬颗粒的补肾壮阳及抗疲劳作用,为其临床用药提供实验依据。方法：通过采用大鼠交配模型和对雄性去势大鼠模型的试验,观察其对大鼠交配能力和时去势大鼠的附性器官、性激素水平的影响。采用氢化可的松致小鼠贤阳虚模型观察其抗疲劳作用。结果：三子强肾混悬颗粒组与模型对照组比较,可显著缩短去势大鼠阴茎勃起潜伏期（P〈0.01）和显著增加大鼠血清睾酮水平（P〈0.01）,可显著增加精囊腺-前列腺,提肛肌质量（P〈0.01）,三子强肾混悬颗粒高剂量组可显著提高正常雄性大鼠的交配能力（P〈0.01）。中、高剂量组均有显著增加肾阳虚小鼠体重及自主活动能力和游泳时间的作用（P〈0.01）。结论：三子强肾混悬颗粒具有较好的补肾壮阳作用及抗疲劳作用。     

蛤蚧的药理作用研究

蛤蚧的乙醇提取物分水溶性(GEHⅠ)和脂溶性(GEHⅡ)两部分。二者对甲醛性大鼠踝关节肿胀,二甲苯所致小鼠耳部炎症及冰醋酸所致腹腔毛细血管通透性增加均具有明显抑制作用,并使幼年大鼠胸腺萎缩,降低正常大鼠肾上腺内维生素C含量,呈现促肾上腺皮质激素样作用。对组胺或乙酰胆碱致痉的豚鼠离体气管平滑肌无松弛作用,也不能对抗蛋清所致的豚鼠过敏性休克。GEHⅡ只能使雄性小鼠睾丸增重,表现出雄性激素样作用,而脂溶性的GEHⅡ对雌性小鼠子宫及雄性小鼠睾丸均可增重。     

色普龙

[通用名称 ]　cyproteroneacetate ,醋酸环丙孕酮[化学名称 ]　 6 氯 1α ,2α 亚甲基 4 ,6 孕甾二烯 17α 羟基 3,2 0 二酮 17 醋酸酯　　 [理化性质 ]　本品为白色或微黄色片剂。[药理作用 ]　本品是一种抗雄激素制剂 ,兼具孕激素和抗促性腺激素样作用 ,因此可抑制垂体促性腺激素的分泌 ,降低血中睾酮的浓度。实验证明 ,本品具有双重抗雄激素作用 ,外周作用可在靶细胞水平竞争结合雄激素受体 ,抑制雄激素活性 ;中枢作用可通过对下丘脑 垂体轴负反馈 ,抑制促性腺激素(LH)分泌 ,使睾酮水平降低 ,降低性欲及性功能 ,减低精子生成量…     

中药阳起石温肾壮阳的作用机理分析

目的探讨阳起石温肾壮阳作用的机理。方法查阅相关文献资料,结合动物实验研究结果进行分析。结果阳起石温肾、壮阳作用相辅相成,与其富含的微量元素有关。结论阳起石的温肾壮阳作用肯定,值得深入研究。     

海马三肾丸补肾壮阳作用实验研究

目的:观察海马三肾丸的补肾壮阳作用,为临床用药提供科学依据.方法:通过对去势雄性大鼠各附性器官重量、雄性大鼠交配能力、阳虚症小鼠抗寒抗疲劳影响的实验研究,观察药物的补肾壮阳作用.结果:药效学实验结果表明海马三肾丸能明显增加阳虚症雄性小鼠耐寒、抗疲劳能力,对去势雄性大鼠各附性器官有明显增重作用,对正常雄性大鼠扑提、射精潜伏期有明显缩短作用.结论:海马三肾丸具有补肾壮阳作用,为临床用药提供科学依据.     

Effect of flutamide on hepatic cytosolic methyltrienolone (R1881) binding kinetics and testosterone responsive hepatic drug and steroid metabolism in the adult male rat

Flutamide was used to investigate the mechanism involved in androgen responsive hepatic microsomal drug and steroid metabolism. We compared the antiandrogenic action of flutamide on the prostate to its effect on testosterone responsive hepatic microsomal benzo[a]pyrene hydroxylase (BPH) and testosterone reductase (TR) activities. Male Wistar rats, castrated as adults, were treated with 5 mumoles.kg-1.day-1 of testosterone enanthate subcutaneously for 10 days. Co-administration of increasing doses of flutamide caused a dose-dependent reduction in prostate to body weight ratios and, in the same animals, caused significant alterations in adult male hepatic microsomal BPH and TR activities. These doses of flutamide did not affect the serum testosterone levels. To test the possibility that the action of flutamide on androgen responsive hepatic microsomal drug and steroid metabolism may be similar to that occurring in the prostate, a tissue which contains an androgen receptor, we also studied the effect of flutamide on the binding kinetics of the high affinity hepatic cytosolic [3H]R1881 binding protein in vivo. Scatchard analysis of [3H]R1881 binding data revealed a reduction in the binding capacity of the hepatic cytosolic androgen binding protein in castrated animals treated with a combination of flutamide and testosterone enanthate at doses capable of maximally altering hepatic microsomal drug and steroid metabolism. No alteration in binding affinity occurred in this treatment group. However, a decreased binding affinity was found when flutamide alone was given. The binding kinetics of the hepatic cytosolic androgen binding protein were not altered in the castrated adult male with or without testosterone treatment. When flutamide was injected daily into the intact adult female rat, no effect was observed on either hepatic microsomal BPH or TR activities. Taken together, these data indicate that flutamide reduces hepatic cytosolic R1881 binding in the adult male rat, and this may explain some of the effects of this antiandrogen on testosterone-sensitive hepatic microsomal drug and steroid metabolism.     

No androgenic/anti-androgenic effects of bisphenol-A in Hershberger assay using immature castrated rats

Several studies have demonstrated that bisphenol A (BPA) exhibited weak estrogenic activity in the 3-day uterotrophic assay using ovariectomized (OVX) and immature rats (Toxicol. Lett. 115 (2000) 231; Regul. Toxicol. Pharmacol. 32 (2000) 118; J. Toxicol. Sci. 26 (2001) 111) and BPA also possessed anti-androgenic activity in in vitro yeast based assays (J. Endocrinol. 158 (1998) 327). To investigate anti-androgenic effects of BPA. a rodent Hershberger assay was carried out using immature Sprague-Dawley male rats. An androgen agonist, testosterone (0.4 mg/kg per day), was administered for 7 consecutive days by subcutaneous (s.c.) injection as a positive control. Additionally, a pure androgen antagonist, flutamide (1, 5. 10 mg/kg per day. oral) was co-administered with testosterone (0.4 mg/kg per day s.c.). BPA was also administered orally with or without testosterone (0.4 mg/kg per day, s.c.) for 7 consecutive days. In the testosterone treated groups, glans penis, seminal vesicles, ventral prostate, and levator ani plus bulbocavernosus muscles (LABC) weights were significantly increased compared with control. However. flulamide dose-dependently inhibited the testosterone-induced re-growth of seminal vesicles, ventral prostate, and LABC, with a significant decrease at flutamide 1.0 mg/kg and above (P<0.05). Serum LH levels were also significantly increased (5 mg/kg and above, P<0.05), but no changes in serum testosterone levels. In contrast, BPA had no effects on the re-growth of seminal vesicles, ventral prostate and LABC induced by testosterone, and no significant differences were observed in serum LH and testosterone levels. In summary, the Hershberger assay could be a sensitive method for detecting androgenic or anti-androgenic chemicals, but BPA did not exhibit any androgenic or anti-androgenic activities in Hershberger assay.     

Prochloraz inhibits testosterone production at dosages below those that affect androgen-dependent organ weights or the onset of puberty in the male Sprague Dawley rat.

Prochloraz (PCZ) is an imidazole fungicide that inhibits gonadal steroidogenesis and antagonizes the androgen receptor (AR). We hypothesized that pubertal exposure to PCZ would reduce testosterone production and delay male rat reproductive development. Sprague Dawley rats were dosed by gavage with 0, 31.3, 62.5, or 125 mg/kg/day of PCZ from postnatal day (PND) 23 to 42 or 51. There was a significant delay in preputial separation (PPS) at 125 mg/kg/day PCZ and several of the androgen-dependent organ weights were decreased significantly, but the significant organ weight effects were not consistent between the 2 necropsies (PND 42 vs. 51). At both ages, serum testosterone levels and ex vivo testosterone release from the testis were significantly decreased whereas serum progesterone and 17alpha-hydroxyprogesterone levels were significantly increased at dose levels below those that affected PPS or reproductive organ weights. The hormone results suggested that PCZ was inhibiting CYP17 activity. In a second pubertal study (0, 3.9, 7.8, 15.6, 31.3, or 62.5 mg/kg/day PCZ), serum testosterone levels and ex vivo testosterone production were significantly reduced at 15.6 mg/kg/day PCZ. In order to examine the AR antagonism effects of PCZ, independent of its effects on testosterone synthesis, castrated immature male rats were dosed with androgen and 0, 15.6, 31.3, 62.5, or 125 mg/kg/day PCZ for 10-11 days (Hershberger assay). In this assay, androgen-sensitive organ weights were only significantly decreased at 125 mg/kg/day PCZ. These data from the pubertal assays demonstrate that PCZ decreases testosterone levels and delays rat pubertal development, as hypothesized. However, the fact that hormone levels were affected at dosage eightfold below that which delayed the onset of puberty suggests that rather large reductions in serum testosterone may be required to delay puberty and consistently reduce androgen-dependent tissue weights.     

Androgen deprivation from pre-puberty to peripuberty interferes in proteins expression in pubertal and adult rat epididymis

Few studies have focused on experimental testosterone deprivation in immature animals. Therefore, this study used sexually immature rats aiming to evaluate the testes and epididymis histology and proteins expression in these organs on PND50 and 75, after premature antiandrogen exposure, from PND21 to 44. Although the androgen deprivation from pre-puberty up to peripuberty did not alter the histological organization of the testes and epididymis either at puberty or at adulthood, the treatment impaired the expression of specific proteins in epididymal tissue at puberty and adulthood (androgen receptor, calmodulin, Rab11A). These changes may be related to impaired epididymal function, sperm quality and fertility capacity as observed in a previous study. Further studies are necessary to better investigate the molecular mechanisms involved in the impairment on reproductive competence of male rats after precocious hormonal injury.     

Sexual dimorphism and the effects of the X-linked Tfm locus on hexobarbitone metabolism and action in mice.

1 Normal males of the testicular feminized strain of mice (Tfm) had longer hexobarbitone-induced sleeping times than females, and hepatic hexobarbitone hydroxylase activity different in that the Km was higher and the Vmax lower in the male. 2 Castration and androgen replacement studies indicated that testicular androgens were responsible for the sexual differences in drug metabolism found in this mouse strain. 3 Hepatic hexobarbitone metabolism and action were feminized in the intact, androgen-insensitive, genetically male Tfm mouse. Furthermore, hexobarbitone hydroxylase activities were less responsive to large doses of testosterone in Tfm mice than in normal males. 4 The Tfm mouse with a deficiency in androgen receptors responded to the enzyme-inductive effects of phenobarbitone and softwood bedding, indicating that these inducers do not act through the androgen receptors.     

Effect of atenolol on cadmium-induced testicular toxicity in male rats

Cadmium-induced stress adversely affects testicular activity and causes sympathetic stimulation. To investigate the effect of atenolol, a β-adrenergic receptor blocker, on testicular androgen synthesis after cadmium treatment, adult Sprague-Dawley strain male rats were given a single sc dose of cadmium chloride 0.45 mg/kg BW. Animals were killed on day 3 after treatment. Adrenal weight, adrenal Δ⁵-3β-hydroxysteroid dehydrogenase (Δ⁵-3β-HSD) activity, serum corticosterone, and brain noradrenaline were increased significantly while testicular Δ⁵-3β-HSD and 17β-HSD activities, serum testosterone, and accessory sex organs weight were decreased. Oral coadministration of atenolol at a dose of 2.0 mg/kg body weight for 3 days resulted in complete protection of adrenal Δ⁵-3β-HSD, testicular Δ⁵-3β-HSD, and 17β-HSD activities, adrenal weight, serum corticosterone, and serum testosterone when compared with cadmium-only group and there were no significant differences in these parameters from the vehicle control values. Simultaneous administration of cadmium and atenolol also protected brain noradrenaline content and reduced the rise of testicular cadmium concentration. All the parameters were similar to control levels in rats treated with atenolol alone. We conclude that atenolol may protect testicular androgen synthesis by inhibiting the action of noradrenaline on testicular Leydig cells and adrenocortical hyperactivity in cadmium-treated rats.     

In Vitro Studies on the Cytotoxic Action of Different Varieties of Asbestos Dust on Macrophages

Abstract: The cytotoxic action of a variety of asbestos dusts viz. chrysotile, amosite, anthophyllite, tremolite and actionlite was tested in vitro using alveolar and peritoneal macrophage cell cultures. The release of acid phosphatase and the uptake of the dye erythrosin B were taken as parameters of cytotoxicity. Among the several varieties of asbestos tested for this purpose, chysotile proved to be most cytotoxic for both the alveolar and peritoneal macrophages, although the former were more sensitive. Amosite was only slightly toxic for alveolar macrophages. Anthophyllite, tremolite and actinolite behaved as control inert dusts. Carboxymethylcellulose exhibited an anticytotoxic effect when chrysotile was pretreated with the polymer or when the dust cell interaction was allowed to take place in its presence.     

Maintenance of sexual behavior in castrate male SW mice using the anti-androgen, cyproterone acetate.

The present study was designed to test the hypothesis that cyproterone acetate (C) might selectively block the actions of dihydrotestosterone (D) and via this action, function as an anti-androgen in male sexual behavior. Sexually experienced male SW mice, a strain previously shown to respond to D following castration, were divided randomly into six groups. Beginning on the day after castration, animals received SC injections for 21 days of either testosterone (T), (D), (C), (T+C), (D+C) or vehicle (V). C was found to significantly reduce seminal vesicle and body weights in all androgen treated groups. There was no evidence to support the contention that C selectively blocks the action of D. To the contrary, in sex tests C maintained palpations, thrust mounts, with intromissions and mounts with ejaculations. Indeed, only animals receiving C alone or in combination with T and D exhibited ejaculations throughout the testing. These results suggest that in the SW mouse, C can work like an androgen in the maintenance of male sexual behavior.     

Sex-related differences in biotransformation of aniline hydroxylase in Sprague-Dawley rats.

A significant difference was found in the rate of aromatic hydroxylation of the type II substrate, aniline, between male and female rats of the Sprague-Dawley strain. In addition, microsomal cytochrome P-450 levels were significantly lower in female rats and aniline-induced spectral binding was significantly greater in microsomes isolated from male rats. Castration caused a significant reduction in aniline metabolism in male rats and testosterone treatment elevated this metabolism toward control level. Treatment of male rats with 17beta-estradiol significantly reduced aniline hydroxylase activity and female rats receiving testosterone for 1 month exhibited significantly increased rates of aniline metabolism over control females. Enzyme activities measured in immature male and in mature and immature female rats were all significantly lower than in mature male rats. These results suggest that the metabolism of aniline in Sprague-Dawley derived rats is controlled by androgen and, thus, is sex-dependent.