本文選題：脾氣虛證 + 小腸運(yùn)動(dòng)　； 參考：《遼寧中醫(yī)藥大學(xué)》2016年碩士論文

【摘要】：目的：研究發(fā)現(xiàn)小腸運(yùn)動(dòng)異常是脾氣虛的常見癥狀,但發(fā)生機(jī)制不甚清楚。血管活性腸肽(vasoactive intestinal peptide, VIP)是一種重要的腦腸肽,其在脾氣虛動(dòng)物模型小腸運(yùn)動(dòng)異常中的作用還有爭(zhēng)議。本工作主要研究脾氣虛時(shí)小腸VIP-VPAC2R-cAMP—PKA信號(hào)轉(zhuǎn)導(dǎo)通路的變化,探討VIP在脾氣虛小腸運(yùn)動(dòng)中的作用。材料與方法：1.動(dòng)物分組20只SPF級(jí)雄性SD大鼠,隨機(jī)地分為對(duì)照組和脾氣虛證模型組(模型組),每組10只。2.模型復(fù)制及評(píng)價(jià)建立飲食失節(jié)加勞倦型脾氣虛模型,即15d內(nèi)：①先飽食1d,再禁食2d,均不禁水,共5個(gè)循環(huán)；②每日水溫35～37℃游泳至力竭。評(píng)價(jià)標(biāo)準(zhǔn)：消瘦,食少,神疲,乏力等。3.小腸運(yùn)動(dòng)評(píng)價(jià)炭末推進(jìn)法測(cè)定大鼠的小腸推進(jìn)率水平。4.小腸形態(tài)學(xué)變化HE染色和透射電鏡觀察小腸的形態(tài)學(xué)變化。5.小腸VIP、cAMP和PKA水平制備小腸組織勻漿,采用ELISA方法檢測(cè)。6.小腸VPAC2表達(dá)免疫組化法觀察大鼠小腸組織中表達(dá)。7.數(shù)據(jù)處理采用SPSS17.0統(tǒng)計(jì)分析軟件分析,實(shí)驗(yàn)數(shù)據(jù)均采用X±S表示,采用t檢驗(yàn),P0.05為有統(tǒng)計(jì)學(xué)有意義。結(jié)果：1.模型評(píng)價(jià)與對(duì)照組相比,模型組大鼠體質(zhì)量、飲食和進(jìn)水量減少,雙前肢抓力下降,在曠場(chǎng)實(shí)驗(yàn)中,對(duì)照組大鼠表現(xiàn)活躍,運(yùn)動(dòng)距離遠(yuǎn),且垂直活動(dòng)次數(shù)多,其活動(dòng)區(qū)域大,反映其好奇程度較高。模型組大鼠反應(yīng)較為遲鈍,運(yùn)動(dòng)距離均顯著縮短,垂直活動(dòng)次數(shù)也降低,活動(dòng)區(qū)域變�。徽f明兩模型組大鼠對(duì)外界事物關(guān)注度降低,好奇程度下降,且反應(yīng)遲鈍,這提示了脾氣虛證大鼠出現(xiàn)了神疲乏力的癥候模型,已經(jīng)導(dǎo)致了脾氣虛證大鼠的中樞神經(jīng)系統(tǒng)嚴(yán)重?fù)p傷。模型組大鼠處于消瘦、納少、神疲和乏力狀態(tài),提示模型復(fù)制成功。2.小腸推進(jìn)率與對(duì)照組相比,模型組大鼠小腸推進(jìn)率明顯降低。3.形態(tài)學(xué)變化光鏡下,與對(duì)照組相比,模型組未見明顯改變；電鏡下,對(duì)照組可見小腸黏膜上皮排列規(guī)則,表面微絨毛豐富,規(guī)則。細(xì)胞核桿狀,形態(tài)較一致,細(xì)胞間緊密連接較短,橋粒結(jié)構(gòu)良好。胞質(zhì)內(nèi)粗面內(nèi)質(zhì)網(wǎng)、線粒體豐富,而模型組黏膜表面上皮排列規(guī)則,胞質(zhì)豐富,表面微絨毛豐富、規(guī)則,明顯變長(zhǎng)。細(xì)胞連接發(fā)育較差,緊密連接短,橋粒豐富,局部胞膜分離。胞質(zhì)內(nèi)含有大量溶酶體,電子密度均勻,粗面內(nèi)質(zhì)網(wǎng)豐富,輕度擴(kuò)張。4.VIP-VPAC2-cAMP-PKA信號(hào)轉(zhuǎn)導(dǎo)通路變化與對(duì)照組比較,模型組大鼠小腸組織的VIP含量顯著升高,而cAMP和PKA的含量均顯著降低,VIP受體在小腸組織的表達(dá)顯著降低。結(jié)論：1.脾氣虛狀態(tài)下小腸運(yùn)動(dòng)減慢與VPAC2R受體表達(dá)下調(diào)所引起的cAMP及PKA的水平下降有關(guān)。
[Abstract]:Objective: the study found that abnormal small intestine movement is a common symptom of spleen qi deficiency, but the mechanism is not clear. Vasoactive intestinal peptide (VP) is an important brain-intestinal peptide, and its role in intestinal motor abnormality of spleen Qi deficiency animal model is still controversial. The purpose of this study was to study the changes of VIP-VPAC2R-cAMP-PKA signal transduction pathway in the small intestine during spleen qi deficiency and to explore the role of VIP in the small intestine movement of spleen qi deficiency. Materials and methods: 1. The animals were divided into 20 SPF male SD rats and randomly divided into two groups: the control group and the model group (model group, 10 rats in each group). The model was duplicated and evaluated to establish the spleen Qi deficiency model of dietetic disconnection and tiredness, that is, within 15 days, 1% 1 fed with full food for 1 day, then fasting 2 days, all could not help water, a total of 5 cycles 2 daily water temperature 3537 鈩，

本文編號(hào)：1810861