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1.
目的:观察雄激素受体(androgen receptor,AR)蛋白及其mRNA在正常组、睾丸切除组和睾丸切除后睾酮替代组大鼠心内神经节的表达及其是否受雄激素的影响.方法:免疫组织化学和原位杂交.结果:三组大鼠心内神经节均存在AR阳性神经细胞,与正常对照组相比,睾丸切除组大鼠心内神经节AR阳性神经细胞数目明显减少,表达明显降低;睾酮替代后AR反应性上升并恢复至正常对照组水平.结论:心房后壁心内神经节存在AR,并且受雄激素调节.  相似文献   

2.
目的 观察雄激素和AR调节剂干预对Seladin-1表达的调控作用,以初步探讨其作用机制.方法 将培养的PC12细胞分为两组:雄激素、AR激动剂组和雄激素、AR阻断剂组,两组均设空白对照组.采用Western-blot和Real-time PCR方法对PC12细胞Seladin-1的表达进行检测.结果 AR激动剂组处理后,PC12细胞Seladin-1的蛋白质与Mrna的表达水平与正常对照组比较均明显提高,差异具有统计学意义(P〈0.05,P〈0.001).AR阻断剂组处理后,PC12细胞Seladin-1的蛋白质与mRNA的表达水平与正常对照组比较均明显降低,差异具有统计学意义(P〈0.05).结论 雄激素和AR参与了PC12细胞Seladin-1表达的调控,雄激素的神经保护效应可能是与通过和AR结合形成激素-受体复合物,并上调seladin-1的表达有关.  相似文献   

3.
外源性GM1对癫痫大鼠脑损伤的保护作用   总被引:7,自引:1,他引:6  
目的 探讨外源性神经节苷脂GM1对癫痫大鼠脑损伤有无保护作用。方法 采用硫代氨基脲 (7.5mg/kg)诱导大鼠癫痫发作模型 ,用免疫组化方法动态观察致痫组大鼠和GM 1干预组大鼠在癫痫发作 2 4小时、4 8小时、72小时及 7天时 ,以及正常对照组、生理盐水组大鼠 72小时时神经生长因子 (NGF)在实验大鼠海马及额叶神经细胞表达情况。同时应用电镜技术观察受损海马神经细胞形态及结构变化。结果 正常对照组和生理盐水组大鼠无癫痫发作 ,致痫组和GM1干预组大鼠有Ⅰ Ⅴ级癫痫发作。免疫组化结果显示 ,癫痫鼠在其海马、额叶有较多的NGF阳性神经细胞表达 ,而未致痫鼠偶有NGF阳性细胞表达 (P <0 .0 5 )。在致痫鼠中 ,GM1干预后NGF表达明显高于未干预组 (P <0 .0 5 ) ,且以 72小时NGF表达为最高(P <0 .0 5 )。电镜显示癫痫鼠神经细胞损伤 ,但GM1干预后损伤减轻 ,而正常对照组和生理盐水组神经细胞形态和结构正常。结论 癫痫发作可引起脑细胞损伤 ;GM1对癫痫大鼠脑损伤具有一定保护作用 ,其保护作用可能通过诱导NGF表达增多来实现。  相似文献   

4.
背景:应用海藻酸钠-多聚赖氨酸-海藻酸钠微囊技术包裹细胞进行异体移植,被证明是一种可避免受体产生免疫排异的有效方法。 目的:观察海藻酸钠-多聚赖氨酸-海藻酸钠微囊化卵巢细胞种植于去卵巢大鼠腹腔后对受体大鼠肾上腺的影响。 设计、时间及地点:随机对照动物实验,于2007-03/2008-09在首都医科大学生殖医学研究中心完成。 材料:取Wistar大鼠卵巢分离培养卵巢细胞,进行微囊化处理,制备包裹卵巢细胞的海藻酸钠-多聚赖氨酸-海藻酸钠微囊。 方法:将40只雌性Wistar大鼠随机分为4组:去势组于无菌条件下切除双侧卵巢;微囊移植组手术摘除双侧卵巢后腹腔移植包裹卵巢细胞的海藻酸钠-多聚赖氨酸-海藻酸钠微囊;雌激素替代治疗组手术摘除双侧卵巢后腹腔注射乙烯雌酚 0.2 mg/kg,每3 d注射1次。正常对照组不进行任何处理。 主要观察指标:干预后30 d放射免疫法检测大鼠血清中雌激素水平,观察肾上腺切片的形态学特点,并利用免疫组织化学SP法检测各组大鼠肾上腺皮质各层增殖细胞核抗原表达变化。 结果:①放射免疫法检测正常对照组,雌激素替代治疗组以及微囊移植组雌激素水平明显高于去势组,而正常对照组,微囊移植组,雌激素替代治疗组之间雌激素水平差异无显著性意义。②去势组肾上腺皮质网状带增厚,网状带与球束状带比值增大,束状带和网状带增殖细胞核抗原阳性表达都增加;而微囊移植组及雌激素替代治疗组增殖细胞核抗原阳性细胞明显低于去势组,差异具有显著性意义。 结论:微囊化大鼠卵巢细胞异体移植后,可在受体大鼠体内继续合成和分泌雌二醇,所分泌的雌激素可以纠正肾上腺皮质因卵巢摘除而导致的形态改变,并与雌激素替代治疗疗效相近。  相似文献   

5.
目的探讨大鼠脊髓在遭受到持续进行性压迫损伤后神经细胞凋亡以及脑源性神经营养因子(BDNF)及其Trk B受体的变化。方法将75只SD大鼠分为模型组、对照组和正常组,各25只;根据造模后取材时间,各组再分为1、7、14、21、28 d 5亚组,每亚组5只。胸11~12椎板和硬脊膜之间置入缓膨材料(3 mm×5 mm,厚0.8 mm)制作大鼠慢性压迫性脊髓损伤模型,BBB评分评估行为学变化,TUNEL染色检测细胞凋亡,免疫组化染色检测BDNF及其Trk B受体表达变化。结果造模后7、14、21、28 d,模型组大鼠BBB评分均明显低于对照组和正常组(P0.05),而对照组和正常组均无统计学差异(P0.05)。模型组大鼠可观察到从脊髓受压开始,神经细胞开始出现凋亡,中央管及前角区域的神经细胞凋亡明显,邻近灰质的白质部分神经胶质细胞凋亡明显;而对照组和正常大鼠未见明显凋亡细胞。模型组大鼠脊髓内BDNF及其Trk B受体呈强阳性,尤其是神经元部位,BDNF及其受体Trk B表达明显,且主要表达在运动类神经元中,随压迫进行,表达逐渐增强,至相对稳定;对照组和正常组大鼠脊髓内BDNF及其Trk B受体表达较少。结论大鼠脊髓在受到慢性压迫性损伤时,神经细胞凋亡明显,BDNF、Trk B受体表达明显增强。  相似文献   

6.
用免疫细胞化学双重标记技术研究雌激素受体(ER)和神经生长因子(NGF)的表达,证实它们在心内神经节共存的可能性。结果显示切片上观察到 3种细胞:(1) ER单标细胞,胞核呈棕褐色;(2 ) NGF单标细胞,胞浆呈红色;(3) ER / NGF双标细胞,胞核棕褐色,胞浆为红色。双标细胞占全部阳性标记细胞的 30%~40%。 这些结果提示ER和NGF可共存于同一大鼠心内神经节细胞,提示雌激素和NGF在维持心内神经节的结构和功能方面存在复杂的交互作用。  相似文献   

7.
目的:探讨丝胶对2型大鼠海马及大脑皮质血红素加氧酶1(HO-1)表达的影响。方法:30只雄性SD大鼠随机分为3组,正常对照组、糖尿病模型组和丝胶治疗组,每组10只。糖尿病模型组和丝胶治疗组大鼠均采用链脲佐菌素连续腹腔注射建立2型糖尿病大鼠模型,以血糖≥16.7mmol/L作为成模标准。待模型成功建立后,模型组大鼠不再作任何处理,丝胶治疗组大鼠给予丝胶(2.4g/kg/d)灌胃35天。HE染色观察海马和大脑皮质的形态变化;分别采用Western Blotting和RT-PCR法检测海马和大脑皮质HO-1蛋白及mRNA的表达。结果:糖尿病模型组大鼠海马及大脑皮质的神经细胞均出现明显的病理变化,HO-1蛋白及mRNA的表达明显高于正常对照组大鼠(P<0.01)。丝胶治疗组大鼠海马、大脑皮质神经细胞的病理变化明显减轻,HO-1蛋白及mRNA的表达明显低于模型组大鼠(P<0.01,P<0.05)。结论:丝胶可通过下调海马及大脑皮质HO-1的表达,减轻糖尿病时HO-1高表达对海马及大脑皮质神经细胞的毒性损害,发挥对糖尿病神经系统损伤的保护作用。  相似文献   

8.
背景:研究表明跑台运动能促进健康大鼠海马的神经细胞再生。 目的:观察跑台运动对脑缺血再灌注模型大鼠海马神经再生和血管内皮生长因子mRNA表达的影响。 方法:用线栓法阻塞大脑中动脉以建立单侧脑缺血再灌注模型大鼠,将建模成功大鼠随机分为跑台运动组和安静对照组,另设假手术组。安静对照组和假手术组大鼠安静饲养,跑台运动组进行7 d跑台运动。跑台运动组和安静对照组大鼠在每天跑台运动前腹腔注射5-溴脱氧尿嘧啶核苷溶液。 结果与结论:免疫组织化学染色结果显示,跑台运动组大鼠双侧海马及齿状回5-溴脱氧尿嘧啶核苷阳性表达细胞数量显著多于安静对照组(P < 0.01)。实时荧光定量PCR检测结果显示,跑台运动组大鼠海马血管内皮生长因子mRNA表达水平显著高于安静对照组和假手术组(P < 0.05)。结果证实,跑台运动能够明显促进脑缺血再灌注大鼠海马神经细胞的再生并上调海马组织血管内皮生长因子的表达。  相似文献   

9.
背景:睾酮对骨关节炎的作用尚无一致的观点,其调节软骨代谢的作用鲜有文献报道。 目的:观察睾酮对膝骨关节炎雄兔关节软骨中胰岛素样生长因子1表达的影响。 方法:24只雄兔随机分成4组,采用改良Hulth法建立右膝骨关节炎模型;假去势组不切除睾丸,其余3组切除双侧睾丸。第8周末处死假去势组和去势8周组兔取材。第9周开始,激素组肌注生理剂量十一酸睾酮(6 mg/kg, 2周1次),去势16周组正常喂养,并于16周末处死并取材。 结果与结论:大体和组织学观察显示各组兔膝关节软骨的病变程度为假去势组优于去势8周组,激素组优于去势16周组。免疫组化染色显示胰岛素样生长因子1在所有兔膝关节软骨中均有表达,阳性细胞个数假去势组高于去势8周组(P < 0.05),激素组高于去势16周组(P < 0.05),去势8周组与去势16周组差异无显著性意义(P > 0.05)。说明睾酮可通过上调去势雄兔关节软骨中胰岛素样生长因子1的表达,延缓软骨退变。  相似文献   

10.
背景:骨质疏松性骨折主要原因是雌激素减少所形成的高转换型骨质疏松,采用雌激素虽能够有效地治疗,但长期雌激素替代治疗会引发诸多疾病。 目的:观察黄精多糖对骨质疏松性骨折大鼠骨代谢因子的影响。 方法:6月龄雌性SD大鼠,随机分为对照组(n=8)和骨质疏松性骨折组(n=36)。骨质疏松性骨折组行卵巢切除后建立骨质疏松性骨折动物模型,再以0.066 mg/kg雌激素,400,200,100 mg/kg 黄精多糖进行灌胃,2 d/次,连续35 d。采用Elisa方法测量骨钙素、抗酒石酸酸性磷酸酶的表达。 结果与结论:骨质疏松性骨折大鼠的骨钙素、抗酒石酸酸性磷酸酶的阳性表达活性升高,给予黄精多糖干预治疗后,高剂量的黄精多糖使骨钙素、抗酒石酸酸性磷酸酶的阳性表达活性下降,而在中、低剂量组干预效果不显著。说明高剂量黄精多糖对骨质疏松性骨折大鼠具有降低骨钙素、抗酒石酸酸性磷酸酶的阳性表达活性的作用,促进骨折愈合的作用。  相似文献   

11.
Androgen might regulate expression of androgen receptors (AR) in AR-containing motoneurons in young animals. In the present study, it was examined whether expression of AR was also regulated by androgen in aged animals. Twelve male rats were castrated at 26 months of age. Five days following castration, the animals were treated with testosterone propionate (TP; six males) or vehicle (six males) and killed 2 hours later. Six sham-castrated rats served as controls. AR immunoreactivity was examined in motoneurons of the spinal nucleus of the bulbocavernosus (SNB) in these animals by immunohistochemistry using the polyclonal antibody PG21. In control animals, slightly intense AR immunoreactivity was confined to the nuclei of the motoneurons. AR immunoreactivity was completely eliminated in the motoneurons of castrated rats. In castrated, aged animals treated with TP, the intensity of AR immunoreactivity in the nuclei of SNB motoneurons was increased. Plasma levels of testosterone in castrated, aged animals 2 hours following treatment with TP were significantly greater than those in controls. These results suggest that expression of AR in motoneurons of the SNB in aged male rats is up-regulated in response to androgen and that androgen may be, at least in part, involved in the process of aging of the SNB in male rats.  相似文献   

12.
Androgenic regulation of androgen receptor (AR) immunoreactivity was examined in androgen-sensitive motoneurons of the spinal nucleus of the bulbocavernosus (SNB) in adult male rats by immunohistochemistry using the polyclonal antibody, PG21. In intact controls, intense AR immunoreactivity was confined to the cell nucleus, but not in the nucleolus of SNB motoneurons, whereas cytoplasmic AR immunoreactivity was weak. Androgen withdrawal significantly reduced both the intensity of AR immunoreactivity in the nuclei and number of AR immunoreactive nuclei of the SNB motoneurons within 1 day of castration. AR immunostaining in the nucleus and cytoplasm was completely eliminated 5 or 10 days following castration. These changes were prevented by replacement of testosterone propionate (TP). The number of AR immunoreactive nuclei recovered to about half of the control levels within 20  min or 1  hr of TP administration to males 5 days after castration, although the intensity of AR immunoreactivity was almost the same as that of males 1 day following castration. Both the intensity of nuclear and cytoplasmic AR immunoreactivity and number of AR immunoreactive nuclei recovered to the control levels 2 or 6  hr after TP injection. These results suggest that androgen causes a significant up-regulation in AR expression of SNB motoneurons.  相似文献   

13.
In some species, including gerbils, guinea pigs, mice, rams and rats, some apparently normal males fail to mate. These kinds of animals have been named 'noncopulating (NC)'. The cause of this behavioural deficit is unknown. The present study aimed to determine whether NC male rats have alterations in the amount of androgen (AR) and oestrogen receptor alpha (ERalpha) in a neuronal circuit important for the control of male sexual behaviour; the vomeronasal projection pathway. We evaluated the number of AR and ERalpha immunoreactive (AR-IR and ERalpha-IR) cells in the accessory olfactory bulb (AOB), the bed nucleus of the stria terminalis (BNST), the anterior-dorsal medial amygdala (MeAD), the posterior dorsal amygdala (MePD) and the medial preoptic area (MPOA). The results demonstrate that the number of AR-IR cells in NC males was significantly higher compared to copulating (C) males in the MePD, but no significant differences were found in any of the other structures analysed. ERalpha-IR cells were more abundant in NC than in C males in the MeAD and the MePD. However, in the MPOA the number of ERalpha-IR cells was significantly reduced in NC males. No significant differences were found in the AOB or in the BNST. A similar pattern of results was observed when regions within these structures that are activated by Fos expression, on mating or exposure to sexually relevant cues were analysed. The differences in the number of AR and ER in particular brain areas could be associated with alterations in sexual behaviour as well as partner and olfactory preference for receptive females seen in NC male rats.  相似文献   

14.
The steroid sensitive vasopressin cells of the bed nucleus of the stria terminalis (BST) and centromedial amygdala (CMA) are involved in numerous behavioural and physiological functions. These cells are known to be greatly influenced by gonadal steroids. Castration reduces and testosterone replacement restores arginine vasopressin (AVP)-immunoreactive (-ir) labelling and AVP mRNA expression in the BST and CMA. Gonadal steroids appear to act directly in AVP-expressing cells within the BST and CMA, because the majority of AVP-ir cells in these areas contain oestrogen and androgen receptor immunoreactivity. Recently, we have localised progestin receptor immunoreactivity in virtually all of the AVP-ir cells in the BST and CMA. To understand the role played by progestin receptors in AVP cells within the BST and CMA, we treated male rats with 1 mg of progesterone or oil for 5 days, and then examined AVP immunoreactivity within the brain. We found that progesterone decreased AVP-ir labelling within the BST and CMA, as well as in two of the projection sites of these cells, the lateral septum and lateral habenula. Progesterone treatment did not alter testosterone secretion from the testes, nor did it alter adult male sexual behaviour. These data illustrate an additional mechanism by which the AVP cells in the BST and CMA can be regulated. These data also suggest that progesterone may act in the male brain to influence behaviours that are AVP-dependent.  相似文献   

15.
Glucose metabolism by aldose reductase (AR) is implicated in the pathogenesis of many diabetic complications, including neuropathy. We have re-evaluated the distribution of AR in the sciatic nerve and dorsal root ganglion (DRG) of normal rats, expanded these observations to describe the location of AR in the spinal cord and footpad skin, and investigated whether diabetes alters the distribution of AR. In sciatic nerve, AR was restricted to cytoplasm of myelinated Schwann cells and endothelial cells of epineurial, but not endoneurial, blood vessels. AR immunoreactivity (IR) was present in satellite cells in the DRG. In skin, AR-IR was detected in vascular endothelial cells, Schwann cells of myelinated fibers, and axons of perivascular sympathetic nerves. AR was localized selectively to oligodendrocytes of the white matter of spinal cord. The distribution of AR-IR in sciatic nerve, DRG, skin, and spinal cord was not altered by up to 12 weeks of streptozotocin-induced diabetes. Identification of perineuronal satellite cells, oligodendrocytes, and perivascular sympathetic nerves as AR-expressing cells reveals them as cellular sites with the potential to contribute to diabetic neuropathy.  相似文献   

16.
Growth hormone (GH) secretory patterns are influenced by gonadal steroids, at least in part, through modulation of hypothalamic somatostatin and GH releasing hormone (GHRH) secretion. In the adult male rat, testosterone appears to stimulate somatostatin gene expression by acting directly on androgen receptors in somatostatin neurones. The mechanism by which gonadal status influences hypothalamic GHRH gene expression is less clear. Gonadectomy reduces GHRH mRNA expression in rats, and this reduction can be prevented by the administration of testosterone or partly by a nonaromatizable androgen. While these observations suggest that androgen receptors mediate the actions of gonadal steroids on GHRH gene expression, they do not provide any information about the location of the androgen receptors involved in this process. To determine whether GHRH neurones themselves express androgen receptors, we double immunolabelled hypothalamic sections from colchicine-pretreated male rats. Although there was an overlap in the anatomical distribution of GHRH and androgen receptor-containing cell bodies, none of the nearly 900 GHRH immunolabelled cells we examined in each mediobasal hypothalamus appeared to contain androgen receptors. These results suggest that GHRH-expressing neurones are not direct targets for androgens and therefore the effects of testosterone on GHRH gene expression must be produced indirectly by some other neural or endocrine intermediary process.  相似文献   

17.
Estrogen (E) regulates a variety of male sociosexual behaviors. We hypothesize that there is a relationship between the distribution of estrogen receptor alpha (ERalpha) and the degree of male social behavior. To test this hypothesis, ERalpha immunoreactivity (IR) was compared in prairie voles (Microtus ochrogaster) from Illinois (IL), which are highly social, and Kansas (KN), which are less social. The expression of androgen receptors (AR) in males also was compared between populations. The expression of ERalpha and AR were compared in brains from KN and IL males and females using immunocytochemistry (ICC). There were significant intrapopulational differences, with males expressing less ERalpha-IR than females in the medial preoptic area, ventromedial nucleus, ventrolateral portion of the hypothalamus, and bed nucleus of the stria terminalis (BST). IL males also displayed less ERalpha-IR in the medial amygdala (MeA) than IL females. While IL males expressed significantly less ERalpha-IR in the BST and MeA than KN males, there was no difference in AR-IR. Differences in the pattern of ERalpha-IR between KN and IL males were behaviorally relevant, as low levels of testosterone (T) were more effective in restoring sexual activity in castrated KN males than IL males. The lack of difference in AR combined with lower expression of ERalpha-IR in IL males suggests that behavioral differences in response to T are associated with aromatization of T to E and that reduced sensitivity to E may facilitate prosocial behavior in males.  相似文献   

18.
Adult hippocampal neurogenesis occurs in many mammalian species. In rats, the survival of new neurones within the hippocampus is modulated by the action of androgen via the androgen receptor (AR); however, it is not known whether this holds true in mice. Furthermore, the evidence is mixed regarding whether androgens act in neural tissue or via peripheral non‐neural targets to promote new neurone survival in the hippocampus. We evaluated whether the action of androgen via AR underlies the survival of new neurones in mice, and investigated whether increasing AR selectively in neural tissue would increase new neurone survival in the hippocampus. We used the cre‐loxP system to overexpress AR only in neural tissues (Nestin‐AR). These males were compared with wild‐type males, as well as control males with 1 of the 2 mutations required for overexpression. Mice were gonadectomised and injected with the DNA synthesis marker, bromodeoxyuridine (BrdU) and for 37 days (following BrdU injection), mice were treated with oil or dihydrotestosterone (DHT). Using immunohistochemistry, proliferation (Ki67) and survival (BrdU) of new neurones were both evaluated in the dorsal and ventral dentate gyrus. Dihydrotestosterone treatment increased the survival of new neurones in the entire hippocampus in wild‐type mice and control mice that only have 1 of 2 necessary mutations for transgenic expression. However, DHT treatment did not increase the survival of new neurones in mice that overexpressed AR in neural tissue. Cell proliferation (Ki67) and cell death (pyknotic cells) were not affected by DHT treatment in wild‐type or transgenic males. These results suggest that androgens act via neural AR to affect hippocampal neurogenesis by promoting cell survival; however, the relationship between androgen dose and new neurone survival is nonlinear.  相似文献   

19.
20.
Gonadal steroids exert important regulatory actions on the hypothalamic neurones regulating growth hormone secretion and are believed to play a role in generating its sexually dimorphic pattern of secretion. Recent evidence indicates that estrogen actions on one of these neural populations, the periventricular somatostatin (SOM) neurones, are likely to be indirect as they do not possess nuclear estrogen receptors in either sex although androgen receptors (ARs) have been reported within these cells in male rats. The present study has used double-labelling immunocytochemistry procedures to examine whether sex differences exist in AR expression by SOM neurones located in the periventricular nucleus and bed nucleus of the stria terminalis (BNST). Within the hypothalamus, SOM-immunoreactive neurones were found concentrated in the periventricular nucleus while both anterior and posterior divisions of the BNST contained scattered populations of SOM cells. Cells immunoreactive for the AR were detected in all of these areas. Although the intensity of AR cell nuclei staining was equivalent in males and females in regions such as the lateral septum, the intensity of AR staining in many individual cells of the periventricular nucleus and posterior BNST of the female was reduced when compared with the male. Double-labelling experiments revealed that approximately 40% of periventricular SOM neurones expressed AR immunoreactivity in the male compared with significantly (P<0.01) fewer cells in the female (~7%). In the BNST, double-labelled cells were only detected within the principle encapsulated, interfascicular and transverse nuclei of its posterior division. Approximately 60% of SOM cells in these nuclei expressed AR immunoreactivity in the male while significantly (P<0.01) fewer did so in the female (~25%). These results indicate that substantial sex differences exist in AR expression by SOM neurones in both the periventricular nucleus and BNST. Such differences in AR expression by periventricular SOM cells may contribute to their sexually dimorphic nature and, consequently, sex differences in growth hormone secretion.  相似文献   

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