本文選題：Mi + RNA-338��； 參考：《內(nèi)蒙古民族大學(xué)》2017年碩士論文

【摘要】：目的:觀察miRNA-338對(duì)實(shí)驗(yàn)性自身免疫性神經(jīng)炎(EAN)模型大鼠的治療作用。方法:30只健康、純系Lewis雌性大鼠隨機(jī)分為三組,即為正常對(duì)照組(n=10)、miRNA-338治療組(n=10)、生理鹽水治療組(n=10);MiRNA-338治療組和生理鹽水治療組大鼠采用P0180-199多肽分別注射雙后肢足底皮下誘導(dǎo)EAN模型。免疫第7天時(shí),從miRNA-338治療組大鼠雙側(cè)坐骨神經(jīng)走行區(qū)選取三個(gè)相同注射位點(diǎn),注射攜帶miRNA-338的慢病毒載體;生理鹽水治療組大鼠相同位置注射相同劑量的生理鹽水;三組大鼠從免疫開(kāi)始記錄行為學(xué)變化并評(píng)分,比較高峰期最高評(píng)分,在免疫后第18天對(duì)各組大鼠進(jìn)行神經(jīng)肌肉動(dòng)作電位、腓腸肌HE染色、運(yùn)動(dòng)終板乙酰膽堿酯酶、甲苯胺藍(lán)染色、坐骨神經(jīng)電鏡組織學(xué)及免疫組織化學(xué)等指標(biāo)檢測(cè),評(píng)估治療效果。結(jié)果:(1)與正常組相比較,miRNA-338治療組行為學(xué)改變接近正常,腳趾握力和行走能力接近正常,高峰期最大平均評(píng)分與生理鹽水治療組組對(duì)比顯著改善(p0.05);(2)與生理鹽水治療組相比較,miRNA-338治療組電生理檢測(cè)顯示高峰期坐骨神經(jīng)復(fù)合動(dòng)作電位傳導(dǎo)速度VmicroRNA-338治療組V生理鹽水治療組(p0.05),振幅AmicroRNA-338治療組A生理鹽水治療組(p0.01);(3)模型動(dòng)物均出現(xiàn):神經(jīng)纖維直徑變小、排列疏松、橫切面形狀不均一,腓腸肌纖維變細(xì)、胞漿淡染,以及運(yùn)動(dòng)終板乙酰膽堿酯酶數(shù)量減少等改變。上述指標(biāo),與生理鹽水治療組相比較,miRNA-338治療組得到明顯改善。(4)電鏡結(jié)果顯示,生理鹽水治療組坐骨神經(jīng)髓鞘出現(xiàn)蜂窩狀改變,髓鞘內(nèi)層與軸索分離剝脫,伴隨軸索變細(xì)等現(xiàn)象,相對(duì)與生理鹽水治療組,miRNA-338治療組剝脫及空洞處可見(jiàn)細(xì)胞修復(fù)的組織結(jié)構(gòu),說(shuō)明miRNA-338對(duì)髓鞘空洞和剝脫有明顯的修復(fù)作用。(5)免疫組化顯示,與生理鹽水治療組比較,miRNA-338治療組高峰期S100和NF200表達(dá)都增高,但S100增高的更為明顯,基本接近正常。結(jié)論:本實(shí)驗(yàn)結(jié)果顯示:1.miRNA-338能明顯改善EAN模型大鼠行為學(xué)評(píng)分、神經(jīng)傳導(dǎo)功能、組織形態(tài)學(xué)等指標(biāo)。2.為臨床尋找新的治療自身免疫炎性疾病提供新思路。
[Abstract]:Aim: to observe the therapeutic effect of miRNA-338 on experimental autoimmune neuritis in rats. Methods Thirty healthy, pure Lewis female rats were randomly divided into three groups: normal control group (n = 10), control group (n = 10) treated with miRNA-338, saline group (n = 10) treated with MiRNA-338 and saline group (n = 30). The EAN model was induced by subcutaneous injection of P0180-199 polypeptide into the foot-floor of both hind limbs. On the 7th day of immunization, three same injection sites were selected from the walking area of bilateral sciatic nerve in the miRNA-338 group, and the lentivirus vector carrying miRNA-338 was injected into the rats of the saline treatment group, and the same dose of normal saline was injected into the rats of the saline treatment group at the same position. The behavioral changes were recorded and scored in the three groups from the beginning of immunity, and the highest score was compared during the peak period. The neuromuscular action potential, HE staining of gastrocnemius muscle and acetylcholinesterase of motor endplate were performed on the 18th day after immunization. Toluidine blue staining, histological and immunohistochemical examination of sciatic nerve were used to evaluate the therapeutic effect. Results compared with the normal group, the behavior changes of miRNA-338 treatment group were close to normal, and the grip strength and walking ability of toes were close to normal. Peak maximum mean score was significantly improved compared with saline treatment group (P 0.05). Compared with saline treatment group, the electrophysiological test of miRNA-338 treatment group showed that the peak period sciatic nerve compound action potential conduction velocity (VmicroRNA-338) treatment group had V birth. Model animals in saline treatment group (P 0.05) and amplitude AmicroRNA-338 group (A normal saline treatment group) all appeared: the diameter of nerve fibers became smaller, The fibers of gastrocnemius became thinner, the cytoplasm was pale, and the number of acetylcholinesterase in motor endplate was decreased. The results of electron microscope showed that the myelin sheath of the sciatic nerve in the saline treatment group was honeycombed, the inner layer of the myelin sheath was separated from the axonal cord, and the axonal cord became thinner. Compared with the normal saline treatment group, the tissue structure of the exfoliation and cavities can be seen in the treated group, indicating that miRNA-338 has obvious repair effect on the cavity of myelin sheath and exfoliation. The expression of S100 and NF200 increased in the peak period of the treatment group compared with that in the saline treatment group, but the expression of S100 was more obvious and close to normal in the control group. Conclusion: the results showed that 1. MiRNA-338 could significantly improve the behavioral score, nerve conduction function and histomorphology of EAN rats. To find a new clinical treatment of autoimmune inflammatory disease to provide a new idea.
【學(xué)位授予單位】：內(nèi)蒙古民族大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類(lèi)號(hào)】：R744.5;R-332

【參考文獻(xiàn)】

相關(guān)期刊論文 前4條

1 陸新華;王輝;寧昕杰;羅駿成;梁家驥;;miR-21在周?chē)窠?jīng)損傷時(shí)調(diào)控雪旺細(xì)胞凋亡[J];中國(guó)病理生理雜志;2015年11期

2 葉曉春;國(guó)海東;田金鑫;牟芳芳;郭春霞;邵水金;;MicroRNA在神經(jīng)損傷修復(fù)中的作用及機(jī)制[J];解剖學(xué)雜志;2015年01期

3 李楠;王建平;蔣超;;CD4~+CD25~+調(diào)節(jié)性T細(xì)胞移植對(duì)實(shí)驗(yàn)性自身免疫性神經(jīng)炎大鼠的保護(hù)作用[J];中國(guó)實(shí)用神經(jīng)疾病雜志;2014年13期

4 楊孫鳳;李淮玉;;細(xì)胞因子與格林巴利綜合征的研究進(jìn)展[J];安徽醫(yī)學(xué);2009年02期

，

本文編號(hào)：1910232