本文選題：雙腎上腺皮質(zhì)激素樣激酶1 + Ki-67　； 參考：《大理大學(xué)》2017年碩士論文

【摘要】：目的:研究胰管結(jié)扎(Pancreatic duct ligation,PDL)術(shù)后雙腎上腺皮質(zhì)激素樣激酶-1(Doublecortin and Ca M kinase-like-1,DCLK1)和增殖細(xì)胞核抗原(Nuclcar-associated antigen,Ki-67)在胰島再生中的表達(dá)及分布,為探討胰島再生的分子調(diào)控機(jī)制提供實(shí)驗(yàn)依據(jù)。方法:隨機(jī)將35只大鼠(體質(zhì)量250±10.8g)分為正常對(duì)照組(5只)和胰管結(jié)扎(PDL)模型組(30只),模型組再分成6個(gè)亞組(每組為5只)。模型組采用4%的水合氯醛腹腔麻醉后于胰尾總管處結(jié)扎主胰管并于術(shù)后1 d、3d、5d、7d、9d、12d分別取胰腺(體、尾部),與對(duì)照組(胰腺體、尾部)進(jìn)行組織學(xué)處理。模型組與對(duì)照組均采用免疫組織化學(xué)SABC染色法觀察DCLK1和Ki-67在胰腺組織中的表達(dá)及分布,并通過(guò)H-E染色,Insulin(Ins)及Glucagon(Glu)免疫染色觀察胰島的再生情況。結(jié)果:DCLK1和Ki-67在正常胰腺組織中存在少量表達(dá),其表達(dá)主要分布在胰腺導(dǎo)管、腺泡和胰島。PDL術(shù)后1、3天,胰腺組織高度水腫,腺泡細(xì)胞變性壞死,胰島形態(tài)被破壞,胰島內(nèi)β細(xì)胞變性壞死,胰島邊緣α細(xì)胞呈Glu免疫陽(yáng)性反應(yīng);DCLK1在胰腺組織內(nèi)呈現(xiàn)異常表達(dá);Ki-67在第3天可見(jiàn)少量免疫陽(yáng)性細(xì)胞,其分布無(wú)特殊。PDL術(shù)后5天,壞死的胰腺組織脂肪化,胰腺小葉內(nèi)的大量腺泡呈脂肪樣變,胰腺小葉內(nèi)開(kāi)始出現(xiàn)管狀復(fù)合體(tubular complexes,TC)結(jié)構(gòu),DCLK1在管狀復(fù)合體上皮呈較強(qiáng)的免疫陽(yáng)性反應(yīng),Ki-67陽(yáng)性細(xì)胞數(shù)量增多較為明顯。PDL術(shù)后7、9天,外分泌部萎縮,許多胰腺小葉被管狀復(fù)合體結(jié)構(gòu)及脂肪組織替代,DCLK1表達(dá)減弱,胰島內(nèi)開(kāi)始出現(xiàn)Ins免疫陽(yáng)性反應(yīng)。PDL術(shù)后12天,胰腺腺泡結(jié)構(gòu)恢復(fù),外分泌部之間出現(xiàn)正常胰島,Ins、Glu免疫陽(yáng)性反應(yīng)較明顯,DCLK1未見(jiàn)表達(dá),Ki-67陽(yáng)性細(xì)胞數(shù)恒定,分布清晰,主要分布在導(dǎo)管、腺泡及胰島,分布具有差異性,差異具有統(tǒng)計(jì)學(xué)意義(P0.05)。結(jié)論:胰管結(jié)扎后,早期胰腺外分泌部組織呈脂肪化,DCLK1異常表達(dá)于TC結(jié)構(gòu);后期DCLK1表達(dá)下降,胰島細(xì)胞形態(tài)及內(nèi)分泌功能恢復(fù)正常。Ki-67陽(yáng)性細(xì)胞分布以導(dǎo)管上皮最為明顯,其次是腺泡及胰島,分布具有差異性。
[Abstract]:Objective: to investigate the expression and distribution of double adrenocorticortin and Ca M kinase-like kinase-1 (DCLK1) and proliferating cell nuclear antigen Nuclcar-associated antigen Ki-67 (PCNA) in islet regeneration after pancreatic duct ligation with Pancreatic duct ligation (PDL). Methods: 35 rats (250 鹵10.8g body weight) were randomly divided into normal control group (n = 5) and pancreatic duct ligation model group (n = 30). The model group was divided into 6 subgroups (5 rats in each group). In the model group, the main pancreatic duct was ligated at the common pancreatic duct after abdominal anesthesia with 4% chloral hydrate, and the pancreas (body and tail) were removed at 1 day, 3 days, 5 days, 7 days and 12 days, respectively, and the control group (pancreatic body, tail) were treated with histology. The expression and distribution of DCLK1 and Ki-67 in pancreatic tissues were observed by immunohistochemical SABC staining in both the model group and the control group. The regeneration of pancreatic islets was observed by H-E staining and Glu-staining. Results there was a small amount of expression of 7% DCLK1 and Ki-67 in normal pancreatic tissues. The expression was mainly distributed in pancreatic ducts, acinar and islet. PDL showed high edema, degeneration and necrosis of acinar cells and destruction of pancreatic islets. 尾 -cell degeneration and necrosis in the islet, Glu immunoreactivity of 偽 cells at the edge of the islet. A small number of immunoreactive cells were found in the pancreatic tissue on the 3rd day, and there was no special expression of Ki-67 on the 5th day after the operation. The necrotic tissue of the pancreas is fatty, and a large number of acinus in the lobules of the pancreas show fatty degeneration. In the pancreatic lobule, the tubular complex (tubular complex TC1) structure began to appear. DCLK1 showed a stronger immunoreactive reaction in the tubular complex epithelium. The number of Ki-67 positive cells increased obviously. The exocrine part shrank 7 days after PDL, and the exocrine part was atrophied at 7 ~ 9 days after PDL. In many pancreatic lobules, the expression of DCLK1 was weakened by tubular complex structure and adipose tissue replacement. The pancreatic acinar structure recovered 12 days after the onset of Ins immunoreactivity in pancreatic islets. The positive expression of Ki-67 was not found in DCLK1. The expression of Ki-67 was distinct in the ducts, acinar and islets. The distribution was different, and the difference was statistically significant (P 0.05). Conclusion: after ligation of pancreatic duct, the tissue of pancreatic exocrine showed abnormal expression of DCLK1 in TC structure in the early stage, the expression of DCLK1 decreased in the later stage, and the morphology and endocrine function of pancreatic islet cells returned to normal. The distribution of Ki-67 positive cells was the most obvious in ductal epithelium. The distribution of acinar and pancreatic islets was different.
【學(xué)位授予單位】：大理大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2017
【分類號(hào)】：R587.1

【參考文獻(xiàn)】

相關(guān)期刊論文 前3條

1 Kenneth Maiese;;Novel nervous and multi-system regenerative therapeutic strategies for diabetes mellitus with mTOR[J];Neural Regeneration Research;2016年03期

2 張麗新;鞠曉芳;王法;郭智偉;樸善花;滕春波;;利用假型反轉(zhuǎn)錄病毒對(duì)大部分胰腺切除后再生細(xì)胞的世系追蹤[J];生物工程學(xué)報(bào);2008年04期

3 李兵,許評(píng),蘇紅,宋春芳;大鼠胰腺導(dǎo)管干細(xì)胞增殖的動(dòng)態(tài)觀察[J];中華實(shí)驗(yàn)外科雜志;2004年03期

，

本文編號(hào)：1803498