發(fā)布時(shí)間：2018-02-24 23:27

  本文關(guān)鍵詞： 慢性非細(xì)菌性前列腺炎 完全弗氏佐劑 BNP NPR-A 疼痛　出處：《南昌大學(xué)》2014年碩士論文　論文類(lèi)型：學(xué)位論文

【摘要】：目的： 建立穩(wěn)定的慢性非細(xì)菌性前列腺炎（CNP）SD大鼠模型。通過(guò)檢測(cè)假手術(shù)對(duì)照組及CNP大鼠模型探討腦鈉尿肽（BNP）及腦鈉尿肽受體(NPR-A)在慢性非細(xì)菌性前列腺炎(CNP)大鼠脊髓背角神經(jīng)節(jié)L6-S1（DRG）中的表達(dá)情況，觀察BNP及NPR-A的表達(dá)變化，以及CNP引起的慢性病理性疼痛與BNP、NPR-A之間的關(guān)系。 方法： 1.本實(shí)驗(yàn)在南昌大學(xué)第一附屬醫(yī)院泌尿外科研究所內(nèi)完成。選擇清潔型SD大鼠100只（全部為雄性），適應(yīng)性飼養(yǎng)1周后，隨機(jī)分為5組分別為：對(duì)照組,向前列腺內(nèi)注射生理鹽水0.1ml;實(shí)驗(yàn)組：3d造模組、7d造模組、10d造模組，14d造模組，向前列腺內(nèi)注射完全弗氏佐劑（CFA）0.1ml構(gòu)建慢性非細(xì)菌性前列腺炎大鼠模型，以上每組均為20只。 2.根據(jù)不同的造模時(shí)間點(diǎn)分別提取對(duì)照組及各個(gè)實(shí)驗(yàn)組SD大鼠的脊髓背角L6-S1段神經(jīng)節(jié)。 3.將其中各組10只的L6-S1神經(jīng)節(jié)段組織中提取RNA，，進(jìn)行逆轉(zhuǎn)錄成cDNA、再行實(shí)時(shí)熒光定量PCR，觀察和計(jì)算在對(duì)照組及造模后各個(gè)時(shí)間點(diǎn)中BNP及NPR-A表達(dá)及其差異，研究BNP、NPR-A在慢性非細(xì)菌性前列腺炎中的表達(dá)、意義及其相關(guān)性。 4.應(yīng)用免疫組化SP方法檢測(cè)另外各組10只的L6-S1神經(jīng)節(jié)中BNP、NPR-A中的表達(dá)及其差異，研究BNP、NPR-A在慢性非細(xì)菌性前列腺炎中的表達(dá)、意義及其相關(guān)性。 結(jié)果： 1.熒光定量PCR所顯示的結(jié)果是BNP在實(shí)驗(yàn)造模組的表達(dá)量比較對(duì)照組均為上調(diào)。3d造模組、7d造模組、10d造模組，14d造模組比較對(duì)照組分別是1.53±0.28倍，2.10±0.32倍，1.85±0.26倍，1.77±0.35倍。熒光定量PCR所顯示的結(jié)果是NPR-A在實(shí)驗(yàn)造模組的表達(dá)量比較對(duì)照組均為上調(diào)。3d造模組、7d造模組、10d造模組，14d造模組比較對(duì)照組分別是1.47±0.21倍，2.05±0.26倍，1.98±0.31倍，1.67±0.23倍。其中7d造模組、10d造模組和14d造模組與對(duì)照組比較差異，有統(tǒng)計(jì)學(xué)意義（P＜0.05）。 2.免疫組化方法所顯示的結(jié)果是BNP及NPR-A在神經(jīng)節(jié)中的神經(jīng)纖維上著色，染色呈紅色，并且在實(shí)驗(yàn)造模組的染色強(qiáng)度高于對(duì)照組。BNP及NPR-A的平均光密度值（OD值）在實(shí)驗(yàn)造模組的表達(dá)量比較對(duì)照組均為上調(diào)。其中7d、10d和14d造模組與對(duì)照組比較差異具有統(tǒng)計(jì)學(xué)意義（*P＜0.05）。 結(jié)論： 利用完全弗氏佐劑（CFA）前列腺注射法建立穩(wěn)定的CNP大鼠模型。BNP及NPR-A在SD大鼠L6-S1神經(jīng)節(jié)中均有表達(dá)，而且造模后形成前列腺炎癥后其表達(dá)均上調(diào)。在CNP導(dǎo)致的疼痛機(jī)制中，BNP及NPR-A有可能參與其中，以及BNP/NPR-A信號(hào)通路在CNP中可能被激活。
[Abstract]:Objective:. A stable rat model of chronic nonbacterial prostatitis was established. To investigate the effect of brain natriuretic peptide (BNP) and brain natriuretic peptide receptor (NPR-A) on the spinal cord of rats with chronic nonbacterial prostatitis (CNP) by detecting the sham operation control group and the CNP rat model. The expression of L6-S1 DRG in hornular ganglion, The expression of BNP and NPR-A and the relationship between chronic pathological pain induced by CNP and NPR-A were observed. Methods:. 1. The experiment was carried out in the Institute of Urology, the first affiliated Hospital of Nanchang University. 100 clean SD rats (all male rats) were randomly divided into 5 groups: control group after one week of adaptive feeding. The rats in the experimental group were injected with normal saline 0.1 ml into the prostate, the experimental group was divided into two groups: the control group (n = 7), the control group (n = 10), the control group (n = 14), and the control group (n = 20) were injected with complete Freund's adjuvant CFAA (0.1 ml) into the prostate to establish the model of chronic non-bacterial prostatitis (n = 20). 2. L6-S1 segment ganglion of spinal dorsal horn was extracted from SD rats of control group and experimental group according to different time points. 3. RNAs were extracted from L6-S1 nerve segments of 10 rats in each group, and then reverse transcripted into cDNAs. The expression and difference of BNP and NPR-A were observed and calculated in the control group and at each time point after modeling. To study the expression, significance and correlation of BNPN NPR-A in chronic nonbacterial prostatitis. 4. Immunohistochemical SP method was used to detect the expression and difference of BNPNPR-A in L6-S1 ganglion, and to study the expression and significance of BNPNPR-A in chronic non-bacterial prostatitis. Results:. 1. The results of fluorescence quantitative PCR showed that the expression of BNP in the experimental model group was higher than that in the control group. The expression of BNP in the control group was 1.53 鹵0.28 times 2.10 鹵0.32 times 1.85 鹵0.26 times 1.77 鹵0.35 times, respectively. The results of PCR showed that the expression of NPR-A in the experimental model group was higher than that in the control group on the 7th day and the 7th day in the control group. The comparison of the control group was 1.47 鹵0.21 times and 2.05 鹵0.26 times and 1.98 鹵0.31 times and 1.67 鹵0.23 times respectively, and the control group was 1.47 鹵0.21 times and 1.98 鹵0.31 times and 1.67 鹵0.23 times respectively. The difference between the control group and the control group was observed. There was statistical significance (P < 0.05). 2. The results of immunohistochemistry showed that BNP and NPR-A were stained on the nerve fibers in the ganglion, and the staining was red. The staining intensity of the experimental model group was higher than that of the control group and the average optical density value (OD value of NPR-A) in the experimental model group, the expression level of the experimental model group was higher than that of the control group, and there was significant difference between the model group and the control group on the 10th and 14th days after 7 days (P < 0.05). Conclusion:. The stable CNP rat model. BNP and NPR-A were expressed in the L6-S1 ganglion of SD rats by using complete Freund's adjuvant CFA-prostatic injection. The expression of BNP and NPR-A may be involved in the pain mechanism induced by CNP, and the BNP/NPR-A signaling pathway may be activated in CNP.
【學(xué)位授予單位】：南昌大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2014
【分類(lèi)號(hào)】：R697.33

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