本文選題：慢性骨盆疼痛綜合征　切入點：CBL/小鼠　出處：《中國實驗動物學(xué)報》2017年03期

【摘要】：目的構(gòu)建慢性骨盆疼痛綜合征前列腺炎(chronic prostatitis/chronic pelvic pain syndrome,CP/CPPS)C57BL/6小鼠模型,探索其機械痛閾和自噬相關(guān)微管輕鏈蛋白LC3和底物蛋白p62表達(dá)水平隨造模時間的變化規(guī)律,為CP/CPPS疼痛及自噬水平研究提供動物實驗依據(jù)。方法將36只雄性C57BL/6小鼠隨機均分為空白組、對照組和模型組,模型組小鼠皮下多點注射大鼠前列腺蛋白提取液和完全弗式佐劑的混懸液,建立CP/CPPS小鼠模型。通過HE染色觀察前列腺病理變化,運用Von Frey纖維絲測定骨盆區(qū)域機械痛閾,通過免疫組化染色檢測LC3和p62表達(dá)水平,運用Image Pro Plus 6.0軟件計算平均光密度。結(jié)果 HE染色可見模型組小鼠出現(xiàn)慢性前列腺炎,表現(xiàn)為不同程度的上皮增生和淋巴細(xì)胞侵潤,且實驗后第6個月前列腺出現(xiàn)上皮內(nèi)瘤(prostatic intraepithelial neoplasia,PIN),表現(xiàn)為基底膜消失和細(xì)胞核異形性明顯等,空白組和對照組則表現(xiàn)為正常組織學(xué)形態(tài)。與空白組及對照組相比,模型組機械痛閾隨造模時間延長逐漸降低[初始痛閾值為(0.35±0.154)g,第22周為(0.008±0.000)g],差異有顯著性(P0.05)。其LC3和p62表達(dá)水平逐漸增高[LC3,p62平均光密度值分別為,第1個月:(2.767±0.464)%,(2.872±1.642)%;第6個月:(13.501±1.900)%,(9.070±0.490)%],差異有顯著性(P0.05)。結(jié)論成功建立了CP/CPPS模型,且造模后第6個月出現(xiàn)PIN。模型組小鼠機械痛閾隨造模時間的延長逐漸降低,LC3和p62表達(dá)逐漸增高,表明CP/CPPS炎癥微環(huán)境促進(jìn)疼痛產(chǎn)生及加劇,并提高小鼠前列腺自噬水平,與PIN的發(fā)生發(fā)展密切相關(guān)。
[Abstract]:Objective to establish a model of chronic prostatitis/chronic pelvic pain pain C57BL / 6 mice with chronic prostatitis/chronic pelvic pain syndrome, and to explore the changes of mechanical pain threshold and the expression level of autophagocyte-associated microtubule light chain protein (LC3) and substrate protein (p62) in mice with chronic pelvic pain syndrome (CPPS / CPPS / C57BL / 6). Methods 36 male C57BL/6 mice were randomly divided into blank group, control group and model group. CP/CPPS mouse model was established by subcutaneous injection of rat prostatic protein extract and suspension of complete Freund adjuvant. The pathological changes of prostate were observed by HE staining, and the mechanical pain threshold of pelvic region was measured by Von Frey filament. The expression levels of LC3 and p62 were detected by immunohistochemical staining, and the mean optical density was calculated by Image Pro Plus 6.0 software. Results chronic prostatitis was found in the model group by HE staining, with different degrees of epithelial hyperplasia and infiltration of lymphocytes. After 6 months, prostatic intraepithelial neoplasia was found in the prostatic prostate, showing the disappearance of the basement membrane and the apparent heteromorphism of the nucleus, while the normal histologic morphology was observed in the blank group and the control group, compared with the blank group and the control group. In the model group, the mechanical pain threshold decreased gradually with the prolongation of the modeling time [the initial pain threshold was 0.35 鹵0.154 g, the initial pain threshold was 0.008 鹵0.000g at the 22nd week], and the difference was significant (P 0.05). In the first month, 2.767 鹵0.464% and 13.501 鹵1.900 鹵9.070 鹵0.490%, respectively, in the first month (2.872 鹵1.642). Conclusion the CP/CPPS model was successfully established, and the mechanical pain threshold of the model group gradually decreased with the prolongation of the model time. The expression of LC3 and p62 increased gradually in the model group. The results showed that the inflammatory microenvironment of CP/CPPS promoted the generation and exacerbation of pain and increased the level of prostatic autophagy in mice, which was closely related to the occurrence and development of PIN.
【作者單位】： 廣西醫(yī)科大學(xué)生命科學(xué)研究院;桂林醫(yī)學(xué)院生物技術(shù)學(xué)院;
【基金】：國家自然科學(xué)基金(項目批準(zhǔn)號:81472414)
【分類號】：R-332;R697.33
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本文編號：1677918