本文關(guān)鍵詞：前列腺素E2EP4受體拮抗劑對大鼠實(shí)驗(yàn)性自身免疫性神經(jīng)炎的影響　出處：《蘇州大學(xué)》2015年碩士論文　論文類型：學(xué)位論文

  更多相關(guān)文章： 前列腺素 L161982 大鼠 免疫性神經(jīng)炎 炎性細(xì)胞因子

【摘要】：目的探討前列腺素E2EP4受體拮抗劑對大鼠實(shí)驗(yàn)性自身免疫性神經(jīng)炎(EAN)的影響,為吉蘭-巴雷綜合征(GBS)尋找新的治療方法。方法選取7~8周齡雌性大鼠18只,建立EAN模型,進(jìn)行臨床評分,按照隨機(jī)數(shù)字表法分成治療A組、治療B組和EAN組各6只,治療A組在免疫前1d至免疫后8d腹腔注射前列腺素E2EP4受體拮抗劑L161982,治療B組在免疫后5~16d腹腔注射L161982,EAN組腹腔注射相同體積的L161982溶媒DMSO+PBS,進(jìn)行組織病理學(xué)檢查和逆轉(zhuǎn)錄聚合式酶聯(lián)反應(yīng)(RT-PCR)技術(shù)檢測,通過CCK8法對體外淋巴細(xì)胞增殖進(jìn)行測定。結(jié)果1.所有大鼠均發(fā)生EAN,且治療A組和治療B組發(fā)病時(shí)間與EAN組比較明顯延遲(P0.05),治療A組與治療B組比較發(fā)病時(shí)間明顯延遲(P0.05);治療A組疾病高峰期臨床評分明顯低于治療B組和EAN組(P0.05)。2.治療A組和治療B組坐骨神經(jīng)血管周圍髓鞘脫失較EAN組明顯減輕(P0.05),組織學(xué)評分較EAN組明顯減少(P0.05),治療A組和治療B組疾病高峰期大鼠淋巴結(jié)炎性細(xì)胞浸潤數(shù)目明顯少于EAN組(P0.05),治療A組大鼠淋巴結(jié)炎性細(xì)胞浸潤數(shù)目明顯少于治療B組(P0.05)。3.治療A組和治療B組在抑制BPM、PHA和ConA誘導(dǎo)的淋巴細(xì)胞增殖方面明顯優(yōu)于EAN組(P0.05)。4.治療A組和治療B組疾病高峰期大鼠淋巴結(jié)炎性細(xì)胞因子TNF-α、IFN-γ、IL-6、IL-17明顯少于EAN組(P0.05),治療A組大鼠淋巴結(jié)炎性細(xì)胞因子TNF-α、IFN-γ、IL-6、IL-17明顯少于治療B組(P0.05)。結(jié)論1.采用L161982治療EAN,無論是在免疫階段還是發(fā)病階段,均能夠明顯降低高峰期臨床評分,延遲EAN發(fā)病時(shí)間,提示L161982能夠治療EAN。2.采用L161982治療EAN,無論是在免疫階段還是發(fā)病階段,均能夠減少淋巴結(jié)炎性細(xì)胞浸潤數(shù)目,降低淋巴結(jié)炎性細(xì)胞因子TNF-α、IFN-γ、IL-6、IL-17表達(dá),提示L161982能夠抑制細(xì)胞免疫反應(yīng)。3.L161982治療免疫階段延遲EAN發(fā)病時(shí)間和疾病高峰期臨床評分明顯優(yōu)于治療發(fā)病階段,提示前列腺素E2EP4受體拮抗劑應(yīng)用于免疫階段效果優(yōu)于發(fā)病階段。
[Abstract]:Objective to investigate the prostaglandin E2EP4 receptor antagonist on rat experimental autoimmune neuritis (EAN) effect for Guillain Barre syndrome (GBS) looking for new treatment methods. Methods 7~8 week old female 18 rats to establish EAN model, clinical score, were randomly divided into treatment group A, treatment group B and EAN group with 6 rats in each treatment group A in immune 1D before and 8D after immunization by intraperitoneal injection of prostaglandin E2EP4 receptor antagonist L161982, treatment group B in immune after intraperitoneal injection of 5~16d L161982, EAN group was intraperitoneally injected with the same volume of L161982 solvent DMSO+PBS, histopathological examination and polymerase chain reaction (RT RT-PCR) detection on lymphocyte proliferation in vitro was determined by CCK8 method. Results 1. all the rats developed EAN, and the time of onset in group A and group B was significantly longer than that in group EAN (P0.05). The time of onset in the treatment group was significantly delayed compared with that in the treatment group (P0.05), and the clinical score in the treatment group was significantly lower than that in the treatment group and the EAN group (A). 2. treatment group A and treatment group B sciatic nerve demyelination around blood vessels significantly reduced compared with EAN group (P0.05), histological score was less than that in group EAN (P0.05), inflammatory cells in treatment group A and treatment group B disease peak rat invasion number was significantly less than in group EAN (P0.05), inflammatory cells in the treatment of A group of rats was significantly less than the number of invasive treatment group B (P0.05). 3. in group A and group B, the proliferation of lymphocytes induced by BPM, PHA and ConA was significantly better than that in group EAN (P0.05). 4., in the A group and the B group, the inflammatory cytokines TNF-, IFN-, IL-6 and IL-17 were significantly less than those in the EAN group (P0.05) at the peak stage of the disease, and the inflammatory cytokines in the A group were significantly less than those in the treatment group. Conclusion 1. the use of L161982 in the treatment of EAN, both in the immune stage or in the onset stage, can significantly reduce the peak clinical score and delay the onset time of EAN, suggesting that L161982 can treat EAN. 2., using L161982 to treat EAN, both in the immune stage or in the onset stage, can reduce the number of inflammatory cell infiltration and decrease the expression of TNF-, IFN-, IL-6 and IL-17, suggesting that L161982 can inhibit the cellular immune response. 3.L161982 treatment delayed the onset time of EAN and the peak of disease. The clinical score was significantly better than that of the treatment stage, suggesting that the prostaglandin E2EP4 receptor antagonist used in the immune stage is better than the onset stage.
【學(xué)位授予單位】：蘇州大學(xué)
【學(xué)位級別】：碩士
【學(xué)位授予年份】：2015
【分類號】：R745.43

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