雙腎上腺皮質激素樣激酶-1和Ki-67在胰管結扎后胰島再生中的表達及分布
發(fā)布時間:2018-04-25 23:32
本文選題:雙腎上腺皮質激素樣激酶1 + Ki-67; 參考:《大理大學》2017年碩士論文
【摘要】:目的:研究胰管結扎(Pancreatic duct ligation,PDL)術后雙腎上腺皮質激素樣激酶-1(Doublecortin and Ca M kinase-like-1,DCLK1)和增殖細胞核抗原(Nuclcar-associated antigen,Ki-67)在胰島再生中的表達及分布,為探討胰島再生的分子調(diào)控機制提供實驗依據(jù)。方法:隨機將35只大鼠(體質量250±10.8g)分為正常對照組(5只)和胰管結扎(PDL)模型組(30只),模型組再分成6個亞組(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扎主胰管并于術后1 d、3d、5d、7d、9d、12d分別取胰腺(體、尾部),與對照組(胰腺體、尾部)進行組織學處理。模型組與對照組均采用免疫組織化學SABC染色法觀察DCLK1和Ki-67在胰腺組織中的表達及分布,并通過H-E染色,Insulin(Ins)及Glucagon(Glu)免疫染色觀察胰島的再生情況。結果:DCLK1和Ki-67在正常胰腺組織中存在少量表達,其表達主要分布在胰腺導管、腺泡和胰島。PDL術后1、3天,胰腺組織高度水腫,腺泡細胞變性壞死,胰島形態(tài)被破壞,胰島內(nèi)β細胞變性壞死,胰島邊緣α細胞呈Glu免疫陽性反應;DCLK1在胰腺組織內(nèi)呈現(xiàn)異常表達;Ki-67在第3天可見少量免疫陽性細胞,其分布無特殊。PDL術后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)開始出現(xiàn)管狀復合體(tubular complexes,TC)結構,DCLK1在管狀復合體上皮呈較強的免疫陽性反應,Ki-67陽性細胞數(shù)量增多較為明顯。PDL術后7、9天,外分泌部萎縮,許多胰腺小葉被管狀復合體結構及脂肪組織替代,DCLK1表達減弱,胰島內(nèi)開始出現(xiàn)Ins免疫陽性反應。PDL術后12天,胰腺腺泡結構恢復,外分泌部之間出現(xiàn)正常胰島,Ins、Glu免疫陽性反應較明顯,DCLK1未見表達,Ki-67陽性細胞數(shù)恒定,分布清晰,主要分布在導管、腺泡及胰島,分布具有差異性,差異具有統(tǒng)計學意義(P0.05)。結論:胰管結扎后,早期胰腺外分泌部組織呈脂肪化,DCLK1異常表達于TC結構;后期DCLK1表達下降,胰島細胞形態(tài)及內(nèi)分泌功能恢復正常。Ki-67陽性細胞分布以導管上皮最為明顯,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.
【學位授予單位】:大理大學
【學位級別】:碩士
【學位授予年份】:2017
【分類號】:R587.1
【參考文獻】
相關期刊論文 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;;利用假型反轉錄病毒對大部分胰腺切除后再生細胞的世系追蹤[J];生物工程學報;2008年04期
3 李兵,許評,蘇紅,宋春芳;大鼠胰腺導管干細胞增殖的動態(tài)觀察[J];中華實驗外科雜志;2004年03期
,本文編號:1803498
本文鏈接:http://www.sikaile.net/yixuelunwen/nfm/1803498.html
最近更新
教材專著