發(fā)布時(shí)間：2018-06-06 04:36

  本文選題：膽囊結(jié)石 + 膽囊動(dòng)力��； 參考：《南京醫(yī)科大學(xué)》2014年博士論文

【摘要】：[研究背景和目的]膽囊結(jié)石是消化系統(tǒng)常見病,其發(fā)病率逐年上升。膽囊結(jié)石分為膽固醇結(jié)石(cholesterol gallstone, CG)及膽色素結(jié)石,其中70%為CG。膽囊動(dòng)力障礙、膽汁淤積是膽囊結(jié)石特別是CG的重要成因,也是保膽治療術(shù)后結(jié)石復(fù)發(fā)的重要原因。Cajal間質(zhì)細(xì)胞(interstitial cells of Cajal, ICC)是胃腸起搏細(xì)胞,其數(shù)量結(jié)構(gòu)或功能異常與許多胃腸疾病密切相關(guān)；ICC的特異標(biāo)志為酪氨酸激酶受體c-Kit,被廣泛用于鑒定ICC及其功能研究。近年來,隨著人膽囊及膽道ICC的發(fā)現(xiàn),ICC在膽囊及膽道中所起的作用倍受關(guān)注。2013年,有研究報(bào)道,膽囊結(jié)石患者膽囊壁ICC顯著減少,提示ICC損害可能參與了膽囊結(jié)石的發(fā)生過程。但膽囊壁ICC損害是否介導(dǎo)了膽囊動(dòng)力障礙而參與膽囊結(jié)石形成?其機(jī)制鮮有報(bào)道。膽囊收縮素(cholecystokinin, CCK)是膽囊收縮的主要激素,血清CCK濃度降低、膽囊CCK1受體(Type 1 cholecystokinin receptor, CCK1)表達(dá)減少與膽囊動(dòng)力障礙、結(jié)石形成密切相關(guān)。近年研究表明,ICC可能是CCK的重要靶細(xì)胞：有研究報(bào)道,大鼠胃幽門ICC及豚鼠的膽囊ICC均表達(dá)CCK1。因此本研究通過：①臨床膽囊標(biāo)本：探討膽囊ICC損害與膽囊動(dòng)力障礙有無相關(guān)性,同時(shí)研究ICC減少是否可引起CCK1減少；②動(dòng)物模型：探討膽囊ICC損害在膽囊動(dòng)力障礙、結(jié)石形成中的作用,及長期高膽固醇飲食對膽囊ICC的影響；③細(xì)胞實(shí)驗(yàn)：高濃度膽固醇對ICC生長的作用,以期闡明CG患者膽囊ICC損害的機(jī)制。[方法]1、臨床標(biāo)本：CG患者膽囊ICC損害與膽囊動(dòng)力障礙的相關(guān)性實(shí)驗(yàn)組：CG膽囊切除患者,對照組：早期胰頭癌或肝右葉肝癌未累積膽囊而行膽囊切除患者。膽囊切除后,取部分膽囊體部組織及膽汁,進(jìn)行以下實(shí)驗(yàn)：(1)免疫熒光雙標(biāo),鑒定人膽囊ICC上是否存在CCK1；(2)制備離體膽囊平滑肌肌條、記錄膽囊肌條的收縮功能；(3)免疫組化標(biāo)記c-Kit+細(xì)胞,免疫熒光雙標(biāo)技術(shù)標(biāo)記ICC,計(jì)算c-Kit+細(xì)胞及ICC密度；將c-Kit+細(xì)胞密度、ICC密度分別與膽囊肌條收縮功能進(jìn)行相關(guān)性分析；(4)免疫熒光雙標(biāo),標(biāo)記CCK1及c-Kit,觀察CCK1表達(dá)與c-Kit表達(dá)間的關(guān)系；(5)HE染色,測量膽囊粘膜層+肌層厚度；Western檢測c-Kit蛋白表達(dá)；(6)檢測膽汁膽固醇濃度。2、動(dòng)物模型：膽囊ICC損害在膽囊動(dòng)力障礙、CG形成中的作用(1)按照文獻(xiàn),建立CG豚鼠模型：4周齡豚鼠40只,隨機(jī)分配至“普通飼料組(Regular diet, RD)"及“致石飼料組(lithogenic diet, LD)";(2)B超監(jiān)測成石情況,喂養(yǎng)6周處死豚鼠,觀察膽囊大體標(biāo)本情況；(3)檢測豚鼠膽囊肌條的收縮功能;(4) real-time PCR檢測c-Kit、CCK1 mRNA表達(dá)；對膽囊肌條收縮功能及c-Kit mRNA表達(dá)水平進(jìn)行相關(guān)性分析。3、細(xì)胞實(shí)驗(yàn)： CG膽囊ICC損害的機(jī)制——高濃度膽固醇對ICC生長的影響(1)酶解法分離小鼠膽囊細(xì)胞,標(biāo)記以下抗體：PE-Cy7(PC7)標(biāo)記的抗c-Kit、PC5標(biāo)記的抗CD45、PC5標(biāo)記的抗F4/80、PC5標(biāo)記的抗CD11b、PE標(biāo)記的抗CD34抗體,流式細(xì)胞儀分選出c-Kit+CD45-F4/80-CD11b-CD34-的細(xì)胞(即具有成熟ICC標(biāo)志的細(xì)胞)；將分選出的細(xì)胞接種至鼠尾膠原包被的培養(yǎng)皿中、含高濃度血清(15%胎牛血清)的M199培養(yǎng)基進(jìn)行培養(yǎng)；(2) Real-time PCR鑒定分選效率、免疫熒光鑒定ICC；(3)細(xì)胞分組：對照組、實(shí)驗(yàn)組(給予不同濃度的水溶性膽固醇(water-soluble cholesterol,WSC));培養(yǎng)72h,real-time PCR檢測c-Kit mRNA水平。[結(jié)果]1、臨床標(biāo)本研究：CG膽囊ICC損害與膽囊動(dòng)力障礙的相關(guān)性(1)對照組(n=10例),CG組(n=30例)。兩組患者平均年齡與男女性別構(gòu)成比均無統(tǒng)計(jì)學(xué)差異(2)人膽囊ICC上存在CCK1表達(dá)(3)CG組離體膽囊肌條收縮能力較對照組明顯減弱(4)CG組膽囊壁c-Kit+細(xì)胞密度及ICC密度均較對照組顯著降低；c-Kit+密度/ICC密度與膽囊肌條收縮能力呈正相關(guān)(5)CCK1表達(dá)與c-Kit表達(dá)變化一致(6)CG組膽囊壁厚度較對照組增厚,膽囊c-Kit蛋白表達(dá)較對照組降低(7)CG組膽汁膽固醇濃度較對照組升高2.動(dòng)物模型研究：膽囊ICC損害在膽囊動(dòng)力障礙、CG形成中的作用(1)RD組豚鼠均未形成膽囊結(jié)石,LD組豚鼠成石率為60%(2)LD組(形成結(jié)石及未形成結(jié)石的)其離體膽囊肌條收縮能力均較RD組減弱(3)LD組豚鼠膽囊c-Kit、CCK1 mRNA表達(dá)較RD組明顯降低(4)膽囊c-Kit mRNA表達(dá)水平與膽囊肌條收縮能力呈正相關(guān)3、細(xì)胞實(shí)驗(yàn)：CG膽囊壁ICC損害機(jī)制——高濃度膽固醇對ICC生長的影響(1)流式細(xì)胞術(shù)分選ICC：具有成熟ICC標(biāo)志的細(xì)胞占全部酶解法分離出的小鼠膽囊細(xì)胞的10.32±2.21%(2)ICC的培養(yǎng)與鑒定：培養(yǎng)12小時(shí)后,可見細(xì)胞貼壁；c-Kit及ANO1 (ICC另一特異標(biāo)志)免疫熒光染色顯示：細(xì)胞c-Kit、ANO1表達(dá)均為陽性,c-Kit標(biāo)記時(shí)細(xì)胞胞質(zhì)著色,ANO1標(biāo)記時(shí)胞質(zhì)及胞核均著色。收集分選前及分選后的ICC進(jìn)行real-time PCR檢測分選效率,結(jié)果提示：分選后的c-Kit mRNA與GAPDH mRNA的比率較分選前提高102±3.18倍(3)外源性WSC干預(yù)：加入10mM、20mmM、40mM的WSC作用72h后,與對照組相比,ICC數(shù)量顯著減少,c-Kit mRNA表達(dá)水平顯著降低(P0.05)[結(jié)論]1、臨床標(biāo)本(CG患者及對照組膽囊、膽汁標(biāo)本)的研究提示：①人膽囊ICC存在CCK1表達(dá),CCK通過作用于ICC表面的CCK1使膽囊收縮；②膽囊壁ICC損害可致CCK1表達(dá)減少,CCK對膽囊收縮作用減弱,進(jìn)而引起膽囊動(dòng)力障礙；③CG患者膽汁中膽固醇濃度較對照組增高。2.動(dòng)物實(shí)驗(yàn)(膽囊膽固醇結(jié)石豚鼠模型)的研究提示：長期高膽固醇攝入可致膽囊ICC減少、膽囊動(dòng)力障礙、進(jìn)而促進(jìn)膽固醇結(jié)石的形成；在結(jié)石形成前,即發(fā)生膽囊動(dòng)力減弱。3.細(xì)胞研究提示：高濃度膽固醇可顯著抑制ICC的生長,CG患者膽囊的ICC損害可能由于長期的高濃度膽固醇膽汁所致。一、研究背景和目的ICC是胃腸起搏細(xì)胞,產(chǎn)生慢波并傳導(dǎo)電興奮,ICC起搏功能的產(chǎn)生與胞內(nèi)Ca2+振蕩有關(guān)。CCK是一種雙重分布在胃腸道及中樞神經(jīng)系統(tǒng)中的腦腸肽,通過其受體對胃腸運(yùn)動(dòng)、膽囊收縮和胰酶分泌等起重要調(diào)節(jié)作用。既往研究發(fā)現(xiàn)大鼠胃幽門ICC上存在CCK1,提示CCK可能直接作用于ICC。本研究首先通過小鼠胃竇組織全層鋪片及切片的c-Kit與CCK1免疫熒光共同標(biāo)記,來證明小鼠胃竇ICC存在CCK1；其次通過分離并培養(yǎng)小鼠胃竇ICC,觀察CCK對ICC胞內(nèi)鈣振蕩的影響,并探討具體的分子機(jī)制。二、方法1、對小鼠胃竇組織全層鋪片、切片及體外培養(yǎng)ICC進(jìn)行c-Kit與CCK1免疫熒光雙標(biāo)2、CCK對ICC胞內(nèi)鈣離子振蕩影響的檢測：(1)酶法分離、流式分選、培養(yǎng)并鑒定小鼠胃竇ICC;(2) Fluo-3/AM負(fù)載ICC,激光共聚焦顯微鏡下觀察CCK、CCK1受體拮抗劑氯戊米特、內(nèi)質(zhì)網(wǎng)鈣泵拮抗劑毒胡蘿卜素、1,4,5-三磷酸肌醇受體(1,4,5-triphosphate, InsP3R)拮抗劑Xestospongin C及L-型Ca2+通道阻滯劑硝苯地平等對ICC胞內(nèi)鈣振蕩的影響。三、結(jié)果1、小鼠胃竇組織、體外培養(yǎng)ICC存在c-Kit與CCK1共定位,免疫熒光鑒定培養(yǎng)的細(xì)胞為ICC;2、CCK對ICC胞內(nèi)鈣離子振蕩影響的檢測：CCK可顯著升高ICC胞內(nèi)鈣離子濃度(intracellular calcium concentration,[Ca2+]i),該效應(yīng)可分別被氯戊米特、毒胡蘿卜素、Xestospongin C所拮抗,給予硝苯地平也可稍減弱CCK的作用。四、結(jié)論CCK通過作用于ICC表面上CCK1受體促進(jìn)其內(nèi)質(zhì)網(wǎng)上InsP3R介導(dǎo)的內(nèi)鈣釋放,導(dǎo)致ICC胞內(nèi)[Ca2+]i顯著升高。
[Abstract]:Cholecystolithiasis is a common disease of digestive system. The incidence of cholecystolithiasis is rising year by year. Gallstone is divided into cholesterol gallstone (CG) and cholelithiasis. 70% of them are CG. gallbladder motility disorder. Cholestasis is the important cause of gallstone, especially CG, and it is also important for the recurrence of gallstones. .Cajal interstitial cells of Cajal (ICC) is a gastrointestinal pacing cell whose quantitative structure or dysfunction is closely related to many gastrointestinal diseases. The specific marker of ICC is a tyrosine kinase receptor c-Kit, which is widely used to identify ICC and its functional study. In recent years, with the discovery of human gallbladder and biliary ICC, ICC is in the gallbladder and The role of the biliary tract has attracted much attention for.2013 years. It has been reported that the gallbladder wall of the patients with gallbladder stones decreased significantly, suggesting that ICC damage may be involved in the process of gallstone. But whether the ICC damage of the gallbladder wall is mediated by gallbladder motility disorder and the formation of gallbladder stones? The mechanism is rarely reported. Cholecystokinin (cholecystokinin, CCK) is the main hormone of gallbladder contraction and the decrease of serum CCK concentration. The decrease of CCK1 receptor (Type 1 cholecystokinin receptor, CCK1) is closely related to gallbladder motility disorder and stone formation. In recent years, the study shows that ICC may be an important target cell of CCK: there are research reports, rat gastric pylorus ICC and guinea pig gallbladder ICC all express CCK1. This study was carried out: (1) clinical gallbladder specimens: To investigate whether there is a correlation between gallbladder ICC damage and gallbladder motility disorder, and whether the reduction of ICC can cause CCK1 reduction or not; 2. Animal models: To explore the effect of gallbladder ICC damage on gallbladder motility, the formation of gallstones, and the effect of long-term high cholesterol diet on gallbladder ICC; Experiment: the effect of high concentration of cholesterol on ICC growth in order to clarify the mechanism of ICC damage to the gallbladder in CG patients. [methods]1, clinical specimens: the experimental group on the correlation between ICC damage and gallbladder motility disorders in CG patients: CG cholecystectomy patients, control group: early pancreatic head cancer or liver right lobe liver cancer without gallbladder and cholecystectomy patients. Gallbladder. After excision, taking part of the body tissue and bile of the gallbladder, the following experiments were carried out: (1) whether there was CCK1 on the gall bladder ICC by double immunofluorescence; (2) the contractile function of the isolated gallbladder smooth muscle muscle was prepared and the contractile function of the gallbladder muscle strips was recorded; (3) the immunohistochemical labeling c-Kit+ fine cell, the immunofluorescence double labeling technique marked ICC, and the calculation of c-Kit+ cell and ICC density Degree; correlation analysis of c-Kit+ cell density, ICC density and contractile function of gallbladder muscle strips; (4) double immunofluorescence labeling, labeling CCK1 and c-Kit, and observing the relationship between CCK1 expression and c-Kit expression; (5) HE staining, measuring the thickness of gallbladder mucosa and muscularis layer; Western detected the expression of c-Kit protein; (6) detection of cholesterol concentration.2, movement of bile. Object model: the function of gallbladder ICC damage in the gallbladder dyskinesia and the formation of CG (1) the CG guinea pig model was established according to the literature: 40 guinea pigs of 4 weeks old were randomly assigned to "Regular diet, RD" and "lithogenic diet, LD"); (2) B ultrasonic monitoring of stone formation and feeding the guinea pigs for 6 weeks to observe the gross specimen of the gallbladder (3) detect the contractile function of the gallbladder muscle strips in guinea pigs; (4) real-time PCR detection of c-Kit, CCK1 mRNA expression, the correlation analysis of the contractile function of the gallbladder muscle strips and the level of c-Kit mRNA expression,.3, cell experiment: the mechanism of CG gallbladder ICC damage: the effect of high concentration cholesterol on ICC growth (1) the isolation of mouse gallbladder cells by enzymatic method. The following antibodies: PE-Cy7 (PC7) labeled anti c-Kit, PC5 labeled anti CD45, PC5 labeled anti F4/80, PC5 labeled anti CD11b, PE labeled anti CD34 antibody, flow cytometry was used to select the c-Kit+CD45-F4/80-CD11b-CD34- cells (that is, the cells with mature markers), and the selected cells were inoculated into the culture dish of the rat tail collagen envelope, M199 medium was cultured with high concentration serum (15% fetal bovine serum); (2) Real-time PCR identification efficiency, immunofluorescence identification of ICC; (3) cell grouping: control group, experimental group (given different concentrations of water-soluble cholesterol, WSC); culture 72h, real-time PCR detection c-Kit mRNA level. [results, clinical Specimen study: the correlation between CG gallbladder ICC damage and gallbladder motility disorder (1) control group (n=10), CG group (n=30). The average age of the two groups was not statistically significant (2) there was a CCK1 expression on the ICC of the gallbladder (3) the contractile ability of the gallbladder muscle in the CG group was significantly lower than that in the control group (4) CG group of the gallbladder wall c-Kit+ cell density The density of /ICC and the density of ICC were significantly lower than that of the control group. The density of c-Kit+ density and the contractile ability of gallbladder muscle strips were positively correlated (5) the expression of CCK1 was in accordance with the changes of c-Kit expression (6) the thickness of gallbladder wall in the group CG was thicker than that of the control group, and the expression of c-Kit protein in the gallbladder was lower than that of the control group (7) the cholesterol concentration in the CG group was increased by 2. animal models compared with the control group. The effect of gallbladder ICC damage on gallbladder motility disorder and CG formation (1) the guinea pigs in group RD did not form gallbladder stones, and the rate of stone formation in group LD was 60% (2) LD (formation of stones and no stones), the contractile ability of the isolated gallbladder muscle in the isolated group was lower than that of the RD group (3) the LD group of guinea pig gallbladder c-Kit, and the CCK1 mRNA expression was significantly lower than that in the RD group (4) the cholecystoc-Kit table. There was a positive correlation between the level and the contractile ability of the gallbladder muscle strips. Cell test: the ICC damage mechanism of CG gallbladder wall - the effect of high concentration of cholesterol on the growth of ICC (1) flow cytometry: ICC: the cells with mature ICC markers accounted for 10.32 + 2.21% (2) ICC of the gallbladder cells isolated from the whole enzyme solution and culture and identification: 12 small culture. C-Kit and ANO1 (another specific marker of ICC) immunofluorescence staining showed that the cell c-Kit, ANO1 expression were all positive, the cytoplasm of the cells were stained with c-Kit markers, and the cytoplasm and nucleus were coloured by ANO1 markers. The sorting efficiency of real-time PCR was collected before and after the sorting, and the results showed: c-Ki after sorting. The ratio of t mRNA and GAPDH mRNA increased by 102 + 3.18 times (3) exogenous WSC intervention: after adding 10mM, 20mmM, 40mM's WSC action 72h, the ICC quantity decreased significantly compared with the control group. The expression of CCK1 in C, CCK through the action of CCK1 on the ICC surface to constrict the gallbladder; (2) the ICC damage of the gallbladder wall may reduce the expression of CCK1, and the contraction of the gallbladder decreases with CCK, and then causes the gallbladder motility disorder; (3) the study of cholesterol concentration in the bile of CG patients with.2. animal experiment (the guinea pig model of gallbladder cholesterol stone) suggests that the cholesterol concentration in the bile is higher than that in the control group. Long term high cholesterol intake may lead to gallbladder ICC reduction and gallbladder motility disorder, which further promote the formation of cholesterol gallstones. Before the formation of the gallstones, the occurrence of gallbladder motility weakened.3. cell research suggests that high concentration of cholesterol can significantly inhibit the growth of ICC, and the ICC damage of the gallbladder in CG patients may be caused by long-term high concentration of cholesterol bile. First, research background and objective ICC is a gastrointestinal pacing cell, which produces slow wave and conduction excitation. The production of ICC pacing function is related to the intracellular Ca2+ oscillation..CCK is a double distribution of the brain gut peptide in the gastrointestinal tract and the central nervous system. Through its receptor, it plays an important role in the gastrointestinal motility, gallbladder contraction and the secretion of pancreatin. It was found that there was CCK1 on the ICC of the gastric pylorus in rats, suggesting that CCK may directly affect the ICC. in this study. First, the c-Kit and CCK1 immunofluorescence of the gastric antrum of mice were first labeled with the c-Kit and CCK1 immunofluorescence, to prove that the ICC existed CCK1 in the gastric antrum of mice. Secondly, the effect of CCK on the ICC intracellular calcium oscillation was observed and the effect of CCK on the ICC intracellular calcium oscillation was observed. To discuss the specific molecular mechanism. Two, method 1, the whole layer of the gastric antrum of mice was paved, the c-Kit and CCK1 immunofluorescence double standard 2, the effect of CCK on the intracellular calcium ion oscillation of ICC were detected: (1) enzyme separation, flow sorting, culture and identification of mouse gastric antrum ICC; (2) Fluo-3/AM loaded ICC, and laser confocal microscope to observe CC K, CCK1 receptor antagonist chloropamyl, endoplasmic reticulum calcium pump antagonist venom carotene, 1,4,5- three phosphoric acid inositol receptor (1,4,5-triphosphate, InsP3R) antagonist Xestospongin C and L- type Ca2+ channel blocker nifedipine, and other effects on the intracellular calcium oscillation in ICC. Three. Results 1, mouse gastric antrum tissue, in vitro culture ICC c-Kit and co localization, The cells cultured by immunofluorescence are ICC; 2, CCK can detect the effect of ICC intracellular calcium ion oscillation: CCK can significantly increase the intracellular calcium concentration of ICC (intracellular calcium concentration, [Ca2+]i). This effect can be antagonized by chloropamyl, carotene, Xestospongin C, and nifedipine can also slightly weaken the action of CCK. Four, conclusion CCK can promote the InsP3R mediated calcium release in the endoplasmic reticulum through the action of CCK1 receptors on the ICC surface, resulting in a significant increase in [Ca2+]i in ICC cells.
【學(xué)位授予單位】：南京醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2014
【分類號(hào)】：R575.62

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