Immunohistochemical Analysis of Omi/HtrA2 Expression in Prostate Cancer and Benign Prostatic Hyperplasia

To study the expression and significance of the serine protease Omi/HtrA2 in prostate cancer and benign prostatic hyperplasia. The expression of Omi/HtrA2 was assayed by means of immunohistochemical technique in 41 prostate cancer （Cap）,20 benign prostatic hyperplasia （BPH） and 10 normal prostate （NP） specimens. Omi/HtrA2 expression was positive in 30 （73.17%） prostate cancer specimens, and the positive rate of Omi/HtrA2 was lower in well differentiated than in poorly and moderately differentiated groups （P〈0.05）. By contrast, the cells in normal prostate and benign prostatic hyperplasia groups showed no or weak expression of Omi/HtrA2. Prostate cancer cells in vivo may need Omi/HtrA2 expression for apoptosis, and that Omi/HtrA2 expression might be involved in prostate cancer development.

Inhibitory Effect of Diosgenin on Experimentally Induced Benign Prostatic Hyperplasia in Rats

This study investigated the effect of diosgenin,a natural sapogenin possessing various pharmacological activities,on benign prostatic hyperplasia（BPH） in rats and the possible mechanisms.BPH was established in the castrated rats by subcutaneous injection of testosterone propionate.Animals were randomly divided into four groups（n=10 each）：model group（0.5% sodium carboxymethyl cellulose）;positive control group（3 mg/kg finasteride）;two diosgenin groups（50 and 100 mg/kg）.The drugs were intragastricaly given in each group for consecutive 3 weeks.Another 10 rats with no testicles cut off served as negative controls and they were subcutaneously injected with 0.1 m L olive oil per day and then treated with 0.5% sodium carboxymethylcellulose.After 3-week administration,the prostate index and serum PSA level were determined,and histopathological examination was carried out.The levels of MDA,SOD and GPx in prostates were also measured.Additionally,the expression of Bcl-2,Bax and p53 was examined using Western blotting.The results showed that the prostate index and serum PSA level were significantly decreased,and the pathological changes of the prostate gland were greatly improved in diosgenin groups as compared with the model group.Elevated activities of SOD and GPx,and reduced MDA level were also observed in diosgenin-treated rats.In addition,the expression of Bcl-2 in prostates was down-regulated,whereas that of Bax and p53 was up-regulated in diosgenin-treated rats.These results indicated that diosgenin was effective in inhibiting testosterone propionate-induced prostate enlargement and may be a candidate agent for the treatment of BPH.

Network pharmacology research and experimental verification of Huangqi(Astragalus Radix)and Jinyingzi(Rosae Laevigatae Fructus)in treating benign prostatic hyperplasia

Objective This study aimed to analyze the mechanism of action of Huangqi(Astragalus Radix,HQ)-Jinyingzi(Rosae Laevigatae Fructus,JYZ)in the treatment of benign prostatic hyperplasia(BPH)based on network pharmacology and to verify the prediction through animal experimentation.Methods Based on the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP),Bioinformatics Analysis Tool for Molecular mechANism of Traditional Chinese Medicine(BATMAN-TCM)databases,and literature,the active components and related target genes of HQ and JYZ were screened.The BPH target genes were screened based on the DisGeNET and GeneGards databases,and Excel was used to merge and remove duplicates.The Perl language was used to obtain drug-BPH target genes by intersecting shared target genes.A drug-component-target gene network diagram was constructed using Cytoscape software.The drug-BPH intersection target genes were inputted into the STRING database,and the key target genes were selected according to the degree algorithm.The output formed the basis for Gene Ontology(GO)and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analyses to determine the potential mechanism of HQ and JYZ in BPH treatment.High,medium,and low doses of HQ and JYZ extract were used to intervene in BPH rats,and then the prostate volume,wet weight,and prostate index of the BPH rats were determined.Changes in prostate histopathology and microvessel density(MVD)were evaluated using immunohistochemistry,and the optimal HQ and JYZ extract dose was confirmed.Finally,the optimal dose was used to intervene in a BPH rat model,and AKT1 and VEGF expressions were examined by immunohistochemistry.Results Based on network pharmacology,33 active components and 772 target genes were identified from HQ and JYZ,along with 817 BPH target genes and 112 drug-BPH common target genes.Among them were 10 key target genes,including AKT1,JUN,MAPK1,IL-6,TNF,ESR1,and VEGFA.KEGG enrichment analysis revealed 135 signaling pathways,including PI3K/AKT,IL-17,TNF,p53,MAPK,VEGF,JAK-STAT,and NF-κB pathways.The animal experiment showed that HQ and JYZ significantly improved prostate volume,wet weight,prostate index,and prostate histopathology of BPH rats,reducing MVD.In addition,HQ and JYZ inhibited the expression of AKT1 and VEGF in the prostate tissue of rats,promoted epithelial cell apoptosis,and inhibited angiogenesis,consistent with the prediction.Conclusion The combination of HQ and JYZ is effective for BPH therapy through multi-compound and multi-target collaboration.Its possible mechanism in treating BPH includes regulation of AKT1,VEGF protein,PI3K/Akt,and VEGF signaling pathways related to apoptosis,angiogenesis,and inflammation,with potential for clinical use and research.

The extract of Celtis choseniana Nakai alleviates testosterone-in-duced benign prostatic hyperplasia through inhibiting 5αreductase type 2 and the Akt/NF-κB/AR pathway

Benign prostatic hyperplasia(BPH)is a chronic male disease characterized by the enlarged prostate.Celtis choseniana Nakai(C.choseniana)is medicinally used to alleviate pain,gastric disease,and lung abscess.In this study,the effect of C.choseniana extract on BPH was investigated using testosterone-induced rats.Sprague Dawley rats were divided into five groups:control,BPH(testosterone 5 mg·kg^(−1)),Fina(finasteride 2 mg·kg^(−1)),and C.choseniana(50 and 100 mg·kg^(−1)).After four weeks of TP treatment with finasteride or C.choseniana,prostate weights and DHT levels were measured.In addition,the prostates were histopathologically examined and measured for protein kinase B(Akt)/nuclear factor-κB(NF-κB)/AR signaling,proliferation,apoptosis,and autophagy.Pro-state weight and epithelial thickness were reduced in the C.choseniana groups compared with that in the BPH group.The extract of C.choseniana acted as a 5αreductase inhibitor,reducing DHT levels in the prostate.Furthermore,the extract of C.choseniana blocked the activation of p-Akt,nuclear NF-κB activation and reduced the expression of AR and PSA compared with BPH.Moreover,the ex-pression of Bax,PARP-1,and p53 increased,while the expression of bcl-2 decreased.The present study demonstrated that C.choseni-ana extract alleviated testosterone-induced BPH by suppressing 5αreductase and Akt/NF-κB activation,reducing AR signaling and in-ducing apoptosis and autophagy in the prostate.These results suggested that C.choseniana probably contain potential herbal agents to alleviate BPH.

Qianliening Capsule(前列宁胶囊) Inhibits Human Prostate Cell Growth via Induction of Mitochondrion-Dependent Cell Apoptosis

Objective： To investigate the molecular mechanisms by which Qianliening Capsule （前列宁胶囊,QC） treats benign prostatic hyperplasia （BPH）. Methods： Human prostate stromal cell line WPMY1 was treated with 0, 1, 3 and 5 mg/mL of QC for 24, 48 and 72 h, respectively, in the presence of 10 ng/mL basic fibroblast growth factor （bFGF）. The viability of WPMY1 cells was determined by 3（4,5Dimethylthiazol2yl）2,5diphenyltetrazolium bromide （M＇lr） assay. Cell morphology was observed by phasecontrast microscopy. 4＇,6diamidino2phenylindole （DAPI） staining and fluorescence activated cell sorting （FACS） analysis with AnnexinV/propidium iodide （PI） staining were performed to determine cell apoptosis. The loss of mitochondrial membrane potential was examined by FACS analysis with 5,5＇,6,6＇tetrachloro1 ,l＇,3,3＇tetraethylbenzimidazolylcarbocyadne iodide （JC1） staining. Activation of caspase3 and 9 was evaluated by colorimetric assay. The mRNA and protein expression levels of Bcl2 and Bax were measured by reverse transcription polymerase chain reaction （RTPCR） and Western blotting, respectively. Results： Upon bFGF stimulation, the viability of WPMY1 cells was increased to 122%118% compared with the control cells （P〈0.05）. However, treatment with 15 mg/mL of QC for 24, 48 and 72 h decreased the viability of bFGFsUmulated cells to 80%92%, 59%82%, 36%62% compared with the untreated cells （P〈0.05）. In addition, QC treatment reduced WPMY1 cell density in a dosedependent manner. Moreover, QC treatment dosedependently induced the loss of plasma membrane asymmetry, the nuclear condensation and fragmentation, collapse of mitochondrial membrane potential, activation of caspase9 and caspase3, and increase of proapoptotic Bax/Bcl2 ratio. Conclusion： Promoting mitochondriondependent apoptosis of prostate stromal cells might be one of the mechanisms by which QC treats BPH.

Effect of β Radiation on Bcl-2 and Bax Expressions in Benign Prostate Hyperplasia Tissues

The authors chose specimens from nine normal prostate tissues（NP group）, 15 benign prostate hyperplasia（BPH） prostates（BPH group）, and 35 BPH prostates that had been treated＇with ^90Sr/^90Y Prostatic Hyperplasia Applicator（exposure group）. The expressions of bcl-2 and bax in stroma and epithelia of prostate tissues were demonstrated by means of immunohistochemical staining, and the staining positive rate was semiquantatively determined, so as to observe the expression of bcl-2 and bax genes in the prostate tissues of normal individuals and BPH patients, before and after fl radiation, and to evaluate the influence of fl radiation on bcl-2 and bax expressions. The expressions of gene bcl-2 in the prostate epithelia of NP and BPH are significantly higher than those in the prostate stroma（P〈0.01）. However, the expressions of bcl-2 in the prostate epithelia and stroma of the BPH group are obviously higher than those in the NP group（P〈0.01）. The expression of gene bax in the prostate epithelia of the NP group is higher than that in the BPH group（P〈0.05）. However, bcl-2 expressions in the prostate epithelia and stroma of the BPH group are significantly higher than the bax expressions（P〈0.01）. Compared with those of the NP group, the expressions of bcl-2 in the prostate epithelia and stroma of the exposure group decrease remarkably, even as the expressions of the bax notably increase（P〈0.01）. Thus, the administration of β radiation can remarkably affect bcl-2 and bax gene expressions, to regulate cell apoptosis, in the prostate tissues of BPH.

黄芪多糖调节PI3K/AKT/mTOR信号通路对良性前列腺增生大鼠细胞凋亡的影响

目的:探讨黄芪多糖(APS)调节PI3K/AKT/mTOR信号通路对良性前列腺增生(BPH)大鼠细胞凋亡的影响。方法:通过摘除双侧睾丸联合皮下注射丙酸睾酮建立BPH大鼠模型,并将建模成功的大鼠随机分为BPH组、APS低剂量(APS-低)组(100 mg/kg APS)、APS中剂量(APS-中)组(200 mg/kg APS)、APS高剂量(APS-高)组(400 mg/kg APS)、APS-高+PI3K激活剂-胰岛素生长因子1(IGF-1)组(400 mg/kg APS+5 mg/mL IGF-1),干预结束后,电子天平称量前列腺湿质量,计算前列腺指数;TUNEL染色检测前列腺组织细胞凋亡变化;免疫组化检测凋亡基因Caspase-3表达;Western blotting检测通路相关蛋白及凋亡基因Bcl-2、Bax表达。结果:与假手术组比较,BPH组前列腺组织病理损伤严重,前列腺湿质量及指数、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR、Bcl-2蛋白表达显著增加,凋亡指数、Caspase-3阳性表达、Bax表达显著降低(P<0.05);与BPH组比较,APS-低组、APS-中组、APS-高组病理损伤改善,前列腺湿质量及指数、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR、Bcl-2蛋白表达显著降低,凋亡指数、Caspase-3阳性表达、Bax表达显著增加,不同剂量APS比较差异有统计学意义(P<0.05);与APS-高组比较,APS-高+IGF-1组病理损伤稍加重,前列腺湿质量及指数、p-PI3K/PI3K、p-AKT/AKT、p-mTOR/mTOR、Bcl-2蛋白表达显著增加,凋亡指数、Caspase-3阳性表达、Bax表达显著降低(P<0.05)。结论:APS可通过抑制PI3K/AKT/mTOR信号通路促进BPH大鼠细胞凋亡,有效抑制BPH进展。

中医药治疗良性前列腺增生症的作用机制研究

良性前列腺增生症在泌尿男科的发病率较高,严重影响中老年患者的身心健康。本病发病原因和机制尚未完全明确,中医药治疗良性前列腺增生症的疗效显著,可以通过改善激素内分泌环境、调节生长因子、促使增生细胞凋亡、松弛平滑肌、抗炎和减少氧化应激等多途径、多机制来干预该病的发生发展。现就近年中医药治疗良性前列腺增生的作用机制研究进行总结。

高血压对良性前列腺增生细胞增殖与凋亡的影响

目的:探讨高血压对良性前列腺增生(BPH)细胞增殖与凋亡的影响。 方法:分别采用Ki 67免疫组织化 学染色及核酸末端原位标记技术(TUNEL)对40例单纯BPH和40例BPH合并高血压患者前列腺组织的细胞增殖 指数(proliferativeindex,PI)与凋亡指数(apoptoticindex,AI)进行检测。 结果:在单纯BPH以及BPH合并高血 压组,前列腺上皮和间质细胞的PI均大于AI(P<0.05),且PI与前列腺体积呈正相关(P<0.05)。与单纯BPH组 比较,BPH合并高血压组前列腺上皮和间质细胞的PI明显增高(P<0.05)。在BPH合并高血压组,高血压病程的 长短与前列腺上皮和间质细胞的PI呈正相关(P<0.05)。 结论:高血压尤其是长期高血压状态可促进前列腺 上皮和间质细胞的增殖,进而导致前列腺体积增大。

补肾活血方对良性前列腺增生大鼠前列腺导管系统上皮细胞凋亡的影响

目的:探讨补肾活血方对BPH大鼠前列腺导管系统上皮细胞凋亡的影响及其可能机制。方法:3月龄雄性Wistar大鼠100只,随机分为对照组、去势组、模型组、模型加补肾活血组4组,每组25只。其中模型组、模型加补肾活血组以去势加丙酸睾酮法复制BPH模型。自造模起,模型加补肾活血组给予2.34 g/ml补肾活血方流浸膏灌胃,其余各组予以等体积生理盐水灌胃,共37 d。去势后第38天处死各组大鼠,并留取标本。免疫组化法检测前列腺导管系统转化生长因子-β1(TGF-β1)、α-肌动蛋白分布及阳性细胞数;TUNEL法检测前列腺导管系统上皮细胞凋亡率。结果:与模型组相比,模型加补肾活血组无论前列腺导管近段[(36.42±8.10)%vs(15.28±4.30)%,P<0.01]还是远段[(8.71±2.28)%vs(4.42±2.07)%,P<0.05],TGF-β1阳性细胞百分数均明显升高,但只有近段α-肌动蛋白阳性细胞率高于模型组[(28.14±7.43)%vs(18.28±4.07)%,P<0.01],但仍然低于对照组[(33.57±6.85)%,P<0.05]。与对照组比较,模型组和模型加补肾活血组前列腺腺管远、近段上皮细胞凋亡率均明显下降[远段:17.60±4.86 vs 3.07±1.14(P<0.01)、12.37±2.25(P<0.05);近段:39.42±9.20vs 3.86±1.34(P<0.01)、31.14±5.64(P<0.01)]。与模型组比较,模型加补肾活血组前列腺腺管远、近段上皮细胞凋亡率均明显增高(P<0.01)。结论:补肾活血方可通过上调TGF-β1表达,抑制前列腺导管系统近端的平滑肌数量减少,促进前列腺腺管上皮细胞凋亡,从而有效地抑制了良性前列腺增生。

益气活血消癥方对良性前列腺增生大鼠细胞凋亡的影响

目的观察益气活血消癥方对良性前列腺增生大鼠细胞凋亡的影响,初步探讨其作用机制。方法将60只8周龄雄性SD大鼠随机分为正常组、阳性对照组和消癥方低、中、高剂量组,每组10只。除正常组外,其余各组大鼠均予去势加丙酸睾酮注射法复制前列腺增生模型。正常组和模型组大鼠予生理盐水灌胃,消癥方低、中、高剂量组大鼠分别予益气活血消癥方10、20、40 mg/100 g灌胃,阳性对照组大鼠予癃开颗粒混悬液11 mg/100 g灌胃,1次/d,连续30 d。末次给药24 h后,脱颈处死大鼠,取前列腺组织,免疫组化检测大鼠前列腺组织Bcl-2、Bax蛋白表达。结果与正常组比较,模型组大鼠前列腺组织Bax表达显著降低,Bcl-2表达显著升高;与模型组比较,各给药组大鼠前列腺组织Bax表达显著升高,Bcl-2表达显著降低,且消癥方高剂量组效果最优。结论益气活血消癥方可促进大鼠前列腺组织细胞凋亡,其机制与前列腺组织Bax蛋白表达升高、Bcl-2蛋白表达降低相关,从而改善良性前列腺增生。

癃必消胶囊对体外培养的人前列腺增生间质细胞作用机制的实验研究

目的研究中药癃必消胶囊对体外培养的人前列腺增生间质细胞的作用机制。方法将雄性日本大耳白兔9只随机分为中药高剂量、低剂量组和对照组,每组3只,中药高、低剂量组分别予癃必消胶囊药粉〔2.0g/(kg.d),1.0g/(kg.d)〕灌胃,对照组予等体积生理盐水灌胃。每天灌胃2次,间隔12h,连续3天。采用最后一次灌药3h后的血清加入细胞培养液。将含癃必消胶囊药物的兔血清加入到体外培养的人前列腺增生间质细胞中,采用TUNEL、ELISA、免疫细胞化学等相关技术检测间质细胞的增殖及凋亡水平。采用实时定量RT-PCR等技术,检测转化生长因子β1(TGF-β1)和Smad7在前列腺增生间质细胞中的表达。结果各组细胞增殖均表现出用药时间依赖性,与对照组比较,各用药组细胞增殖水平显著降低,差异有统计学意义(P<0.01),与低剂量组比较,高剂量组增殖降低,差异有统计学意义(P<0.01)。各组培养48h的前列腺间质细胞,在形态上并未出现明显的不良生长状况,各组间差异均无统计学意义。对照组和低剂量组未见凋亡现象,只有高剂量组出现少量凋亡细胞。低、高剂量组TGF-β1、Smad7表达水平均低于对照组,差异均有统计学意义(均P<0.01)。低剂量组与高剂量组比较,差异无统计学意义(P>0.05)。结论癃必消胶囊能降低基因TGF-β1和Smad7的表达,抑制前列腺间质细胞增殖,而对其凋亡无明显的影响。

康泉方对大鼠前列腺组织凋亡调控基因bax、bcl-2mRNA表达的影响

目的探讨康泉方对实验性大鼠前列腺组织凋亡调控基因bax mRNA、bcl-2 mRNA的影响。方法采用大鼠去势后注射丙酸睾丸酮致前列腺增生法造模,同时灌胃给药30天后,处死大鼠取前列腺组织并测量湿重,RT-PCR法检测各组前列腺腹叶组织bax mRNA、bcl-2 mRNA的表达。结果与模型组比较,康泉各剂量组前列腺湿重显著下降(P<0.05或P<0.01);康泉高剂量组前列腺湿重与正常组比较,差异无显著性(P>0.05);与模型组比较,康泉各剂量组bax mRNA及bax/bcl-2显著升高(P<0.01),bcl-2 mRNA显著下降(P<0.01);康泉高剂量组bax mRNA、bcl-2 mRNA及bax/bcl-2与正常组比较,差异无显著性(P>0.05)。结论康泉方对大鼠良性前列腺增生有明显的治疗作用,其作用机理可能通过调节前列腺组织bax mRNA、bcl-2 mRNA表达,促进前列腺细胞凋亡,并呈明显量效关系。

山绿茶总黄酮对BPH模型大鼠前列腺细胞凋亡的影响

用去势大鼠注射丙酸睾酮建立前列腺增生模型,山绿茶总黄酮按80、402、0 mg.(kg.d)-1灌胃4周;分离前列腺组织,匀浆,制备单细胞悬液,流式细胞术测定细胞凋亡率;另取前列腺制备超薄切片,电镜下观察前列腺细胞超微结构,研究山绿茶总黄酮对大鼠前列腺增生模型细胞凋亡和超微结构的影响。结果表明:正常组前列腺细胞无明显凋亡;模型组前列腺细胞凋亡率较低;山绿茶总黄酮高剂量组,大鼠前列腺细胞凋亡率明显增高,与模型组比较,差异极显著(P<0.01)。电子显微镜观察可见,山绿茶总黄酮组前列腺细胞核较完整,细胞核浓缩不明显,但其致密度增高,粗面内质网空泡减少;与对照组比较,超微结构变化不明显。说明山绿茶总黄酮可诱导前列腺细胞凋亡,因而抑制前列腺增生,对其超微结构有明显的改善作用。

癃畅颗粒对睾酮诱导的大鼠前列腺增生组织bax表达影响的研究

目的:通过癃畅颗粒对大鼠前列腺增生组织中bax表达影响的研究,探讨癃畅颗粒治疗前列腺增生的作用机制。方法:采用大鼠去势后注射丙酸睾酮致前列腺增生法造模,灌胃给药后30d处死。摘取前列腺组织并测量湿重,采用免疫组化对癃畅颗粒和癃闭舒干预的大鼠前列腺增生组织进行bax检测。结果:前列腺湿重:空白组(0.61±0.03)g,模型组(0.95±0.04)g,癃闭舒组(0.73±0.02)g,癃畅颗粒低剂量组(0.80±0.05)g,癃畅颗粒中剂量组(0.78±0.07)g,癃畅颗粒高剂量组(0.68±0.03)g,与模型组比较差异有显著性(P<0.05)。前列腺指数:空白组0.143±0.006,模型组0.226±0.008,癃闭舒组0.172±0.004,癃畅颗粒低剂量组0.199±0.012,癃畅颗粒中剂量组0.181±0.010,癃畅颗粒高剂量组0.168±0.003,与模型组比较,差异有显著性(P<0.05)。癃畅颗粒对BPH大鼠前列腺上皮细胞bax表达影响(平均光密度):空白组0.226±0.010,模型组0.184±0.005,癃闭舒组0.206±0.015,癃畅颗粒低剂量组0.199±0.001,癃畅颗粒中剂量组0.202±0.003,癃畅颗粒高剂量组0.211±0.003,与模型组比较,差异有显著性(P<0.05)。结论:癃畅颗粒能够有效缩小模型大鼠前列腺湿重,减轻病理变化。其作用机制可能为上调大鼠前列腺bax基因表达促进前列腺细胞凋亡。

桂枝对大鼠良性前列腺增生细胞增殖和凋亡的影响

目的:研究桂枝对大鼠良性前列腺增生细胞增殖和凋亡的影响。方法:大鼠皮下注射丙酸睾丸素(5mg/kg)造成良性前列腺增生动物模型,经灌胃给以不同剂量桂枝水煎液(6.67g/kg、3.33g/kg和1.67g/kg),阳性对照组相同途径给予保列治(非那雄胺)水溶液(0.45mg/kg),正常对照组和模型组给予等体积离子净化水。30d后处死大鼠,观察大鼠前列腺指数变化,HE染色光镜观察前列腺病理改变,Ki-67免疫组化染色和TUNEL染色检测大鼠前列腺细胞的增殖指数和凋亡指数。结果:桂枝能明显降低大鼠的前列腺指数(P<0.01),明显减轻前列腺组织病理改变,提高前列腺细胞凋亡表达率(P<0.01);而对前列腺细胞增殖指数没有明显作用(P>0.05)。结论:桂枝具有抗大鼠良性前列腺增生的作用,促进大鼠前列腺增生细胞凋亡可能是其机理之一。

Bcl-2基因与良性前列腺增生

B淋巴细胞瘤2(Bcl-2)基因是Bcl-2基因家族的一个重要成员。Bcl-2家族是在细胞凋亡过程中起重要作用的一类蛋白质。Bcl-2基因不改变细胞增殖速度,而是通过抵抗多种形式的细胞死亡延长细胞寿命,导致细胞数目增加。近年来越来越多的证据表明,Bcl-2基因与BPH的发生、发展密切相关。BPH的发病机理至今尚未完全阐明,随着研究的深入,细胞凋亡在其中的作用日益受到重视。本文从Bcl-2基因的抗凋亡机制和其与BPH的关系两方面,就近年来对其研究的最新进展进行综述,以探讨抗凋亡基因Bcl-2在BPH的发生、发展过程中所起的作用。

中医药治疗前列腺增生的药理作用分析

目的:探讨前列腺增生的分子机制及中医药在前列腺增生治疗中的特点。方法:通过对前列腺增生不同发病机制的归纳分析,揭示前列腺增生的分子机制;对前列腺增生的常见治疗方法及药物进行分析,探讨中医药治疗前列腺增生疗效的特点。结果:生长因子学说、激素内分泌学说、细胞凋亡学说是前列腺增生的主要机制,相互交叉,以生长因子学说最为重要;中医药治疗前列腺增生具有明显优势。结论:三个学说相互交叉,从不同角度揭示了前列腺增生的分子机制,中医药可较好防治前列腺增生的发生与发展。

萘哌地尔衍生物BWYJ抗前列腺增生的作用

目的观察萘哌地尔衍生物BWYJ对前列腺增生模型的作用。方法采用激素法建立去势大鼠和未去势小鼠前列腺增生模型,通过小鼠前列腺湿重,计算前列腺指数。光镜及透射电镜下,分别观察小鼠前列腺组织形态学及超微结构变化;TUNEL法检测BWYJ对大鼠前列腺细胞凋亡的影响。结果BWYJ5、10、20mg·kg-1组均可降低BPH小鼠前列腺湿重指数(P<0.05),光镜及电镜结果表明,BWYJ5、10、20mg·kg-1组均可抑制小鼠组织结构增生性变化,且BWYJ10、20mg·kg-1组使腺腔直径、腺体表面积变小(P<0.05)。TUNEL检测发现,大鼠前列腺凋亡细胞检出率较低,与模型组比较,BWYJ各剂量组差异无统计学意义(P>0.05)。结论BWYJ具有抗小鼠及大鼠良性前列腺增生作用。

Caspase-1在良性前列腺增生组织中的表达及意义

目的:探讨正常和良性前列腺增生(BPH)组织中的caspase-1表达情况及意义。方法:应用免疫组化SP法分别检测21例BPH组织和7例正常前列腺组织标本中caspase-1的表达。结果:caspase-1阳性表达率在BPH组织中为71.4%(15/21),正常前列腺组织中为100%(7/7)。BPH上皮组织和间质组织的caspase-1阳性表达均比正常前列腺明显减少(P<0.01)。在BPH组织内部,上皮的caspase-1阳性表达明显高于间质(P<0.01)。结论:caspase-1在BPH组织中的表达较正常前列腺组织显著减少,提示由caspase-1介导的凋亡过程的减少可能参与了BPH的发病过程。