【作者】 樊松；

【导师】 梁朝朝； 叶元平； 刘明；

【作者基本信息】 安徽医科大学 ， 外科学， 2008， 硕士

【摘要】 研究目的探讨研究钙离子通道TRPV5在慢性前列腺炎患者及慢性前列腺炎小鼠前列腺组织中的表达及其意义材料与方法1．收集128例前列腺标本，其中我院2000年1月-2003年12月期间前列腺增生术后标本123例，年龄55-83岁；19岁和22岁男性尸体标本2例；48岁、49岁和51岁全膀胱术后标本3例；使用光学显微镜观察128例前列腺HE切片的组织学特点。选择良性前列腺增生术后标本73例，其中炎症组41例，非炎症组32例，然后调出相应的HE切片和包埋蜡块，病人年龄61-82岁，在光学显微镜下复查HE染色结果。应用SP法对其进行免疫组化染色，检测TRPV5在慢性前列腺炎患者前列腺上皮细胞中的表达。2．根据国内外制作慢性免疫性非细菌性前列腺炎动物模型的经验，摸索优化造模方法，初步建立C57BL／6小鼠的慢性免疫性前列腺炎动物模型。验证造模成功后，应用SP法、Western blot及RT-PCR等方法检测TRPV5在慢性前列腺炎小鼠前列腺组织中的表达。结果1．128例前列腺标本67例腺体内局灶性炎症细胞浸润分布在外周区、移行区和尿道周围区，占52．3％；而中央区无明显的局灶性炎症细胞浸润。5例非前列腺增生组内，3例有局灶性炎症细胞浸润，2例无明显局灶性炎症细胞浸润。χ~2=8．795，P=0．122>0．05，两者间差别无统计学意义。41例炎症组前列腺标本中TRPV5强表达的有22例，中表达的10例，低表达的9例；32例非炎症前列腺标本中TRPV5强表达的有7例，中表达的9例，低表达的16例；χ~2=8．795，P=0．012<0．05，两组间差异有统计学意义。2．造模8周后，C57BL／6小鼠前列腺呈现慢性炎症病理变化，与临床慢性前列腺炎病理变化相似。慢性前列腺炎小鼠前列腺组织TRPV5mRNA呈高表达((?)±s=0．587±0．080)，正常对照组呈低表达((?)±s=0．815±0．062)(P=0．004<0．05)。慢性前列腺炎小鼠前列腺组织中TRPV5蛋白呈高表达((?)±s=0．925±0．053)，正常对照组呈低表达((?)±s=0．733±0．097)(P=0．013<0．05)。结论1．前列腺腺体内的局灶性炎症细胞浸润大多集中于外周区、移行区和尿道周围区，而中央区均无明显的局灶性炎症细胞浸润，这可能与不同区域的腺泡大小、形态、腺管分布、排列和走行密切相关；前列腺腺体内有无炎症细胞浸润与良性前列腺增生也无明确相关性。TRPV5通道在慢性前列腺炎患者前列腺炎症组和非炎症组前列腺标本中前列腺上皮细胞中表达有明显差异，钙通道的改变可以影响细胞生物学行为，引起上皮细胞功能障碍。2．应用免疫造模法建造小鼠慢性前列腺模型，其病理结果与临床慢性前列腺炎病理结果表现相近，为近一步研究慢性前列腺炎的发病机制及寻找有效治疗的新药提供了实验方法。TRPV5在慢性前列腺炎前列腺组织中高表达，提示TRPV5通道的改变可能是慢性前列腺炎的发病机制之一。更多还原

【Abstract】 ObjectiveTo investigate the function of TRPV5 channel in the pathogenesis of Chronic Prostatitis.Methods1. 128 prostate specimens were collected including 123 post-operation of human benign prostate hyperplasia which all came from our hospital during the time of 2000.1-2003.12,55-83 years old; 2 of corpse bodies for renal transplantation, 19 and 22 years old respectively. By using the light microscopy, the 128 hematoxylin-eosin stained slides were observed. Pick out pathological number of the 73 prostate specimens; then apply the methods of the SP immunohistochemisty to detect the expression of TRPV5 in human Prostatic epithelia.2. To develop a mouse model of nonbacterial chronic prostatitis. Through adopting SP、Western blot and RT-PCR to examine the TRPV5 expression of the C57BL/6 mice contracting the experimental nonbacterial chronic prostatitis by comparison of the normal-functioning mice.Results1. Obvious nodular inflammatory cells infiltration in the peripheral zones, transitional zones and periureth gland regions but not in the central zones were observed in 67 among all the 128 prostate specimens, which accounting for the percentage of 52.2.For nodular inflammatory cells infiltration 3 were observed in the 5 non-hyperplasia of prostate, and 64 were observed in the 123 hyperplasia of prostate. There was no statistic difference between the two groups, x~2 =8.795, P =0.122>0.05.Of 41 inflammationgroup, according to TRPV5’s degrees of expression,22 are designated as strong expression; 10 moderate; 9 low; of 32 noninflammation groups, 7 designated as strong;9 moderate; 16 low. There was statistic difference between the two groups (chi-squared, P<0.05).2. After 8 weeks, the prostates of model mice exhibited varying degree of inflammations, and were found to have lymphocytic infiltration of the storma and periglandluar region, which were similar to clinical nonbaterial chronic prostatitis. In opposition to the low expression of TPRV5 proteins and mRNA in NBCP-freemice, the high one has been found in the NBCP bears.Conclusion1. Almost all the obvious nodular inflammatory cells infiltration occur in the peripheral zones, transitional zones and periurethral gland regions but not in the central zones ,which may be closely correlated with the size,shape,distribution,arrange and track of the gland acini and ducts .Histopathologic finding of increased nodular inflammatory cells infiltration within the prostatitis parenchyma can not be recogised the diagnostic level of chronic prostatitis ,and there is no definite correlation between nodular inflammatory cells infiltration with benign prostatic hyperplasia .The expression of the TRPV5 channel was higher in prostatic epithelia cells from patients with chronic inflammation than from those without. The change of the calcium channel can conduce to genesis of Chronic Prostatitis.2. Injection of immunizator ( antigen) and adjuvant can induce prostatic inflammation similar to clinical nonbatenal chronic prostatitis ,which may be an immune process. Itcould bring us a new way for studying pathogenesis of chronic prostatitis and drugtherapy.更多还原