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胆固醇结石患者肝脏羧肽酶E的表达降低。

The expression of hepatic carboxypeptidase E is decreased in patients with cholesterol gallstone.

作者信息

Dai Shu-Long, Zhou Jin, Yang Kun-Xing, Yang Shi-Yong

机构信息

Department of General Surgery, Nanjing First Hospital, Nanjing Medical University, Nanjing 210006, China.

出版信息

Saudi J Gastroenterol. 2015 Jul-Aug;21(4):226-31. doi: 10.4103/1319-3767.161640.

DOI:10.4103/1319-3767.161640
PMID:26228366
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4542421/
Abstract

BACKGROUND/AIMS: Decreased carboxypeptidase E (CPE) expression is associated with numerous pathophysiological conditions. This study aimed to investigate the potential function of hepatic CPE in cholesterol gallstone formation.

PATIENTS AND METHODS

Patients with cholesterol gallstone (CGS group) and patients without cholesterol gallstones (non-CGS group) were enrolled. The serum total cholesterol, triglyceride, and biliary composition were analyzed. Eight liver samples from two patients without CGS and six patients with CGS were subjected to cDNA microarray analysis. Hepatic CPE expression was detected by quantitative real-time polymerase chain reaction (qRT-PCR), Western blot, and immunohistochemical analysis. Plasma CCK level was measured by ELISA.

RESULTS

cDNA microarray identified CPE as a gene downregulated in the CGS group. RT-PCR showed that CPE mRNA level was lower in CGS group than in control (P < 0.05, t-test). Moreover, Western blot and immunohistochemistry analysis showed that CPE protein level was significantly lower in CGS group than in the control group. In addition, plasma CCK level was lower in CGS group than in the control group. A positive correlation was found between serum CCK level and hepatic CPE mRNA level (r2 = 0.713, P = 0.003).

CONCLUSIONS

Down-expression of liver CPE may reduce the secretion of serum CCK and contribute to the formation of cholesterol gallstone.

摘要

背景/目的:羧肽酶E(CPE)表达降低与多种病理生理状况相关。本研究旨在探讨肝脏CPE在胆固醇结石形成中的潜在作用。

患者与方法

纳入胆固醇结石患者(CGS组)和无胆固醇结石患者(非CGS组)。分析血清总胆固醇、甘油三酯和胆汁成分。对2例非CGS患者和6例CGS患者的8份肝脏样本进行cDNA微阵列分析。通过定量实时聚合酶链反应(qRT-PCR)、蛋白质免疫印迹法和免疫组织化学分析检测肝脏CPE表达。采用酶联免疫吸附测定法(ELISA)检测血浆胆囊收缩素(CCK)水平。

结果

cDNA微阵列鉴定CPE为CGS组中下调的基因。RT-PCR显示CGS组中CPE mRNA水平低于对照组(P < 0.05,t检验)。此外,蛋白质免疫印迹法和免疫组织化学分析显示CGS组中CPE蛋白水平显著低于对照组。另外,CGS组血浆CCK水平低于对照组。血清CCK水平与肝脏CPE mRNA水平呈正相关(r2 = 0.713,P = 0.003)。

结论

肝脏CPE的低表达可能会减少血清CCK的分泌并促进胆固醇结石的形成。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1f3/4542421/537a31fe2ceb/SJG-21-226-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1f3/4542421/0c3cc5512793/SJG-21-226-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1f3/4542421/537a31fe2ceb/SJG-21-226-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1f3/4542421/0c3cc5512793/SJG-21-226-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1f3/4542421/537a31fe2ceb/SJG-21-226-g004.jpg

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Roles of cholesterol and bile salts in the pathogenesis of gallbladder hypomotility and inflammation: cholecystitis is not caused by cystic duct obstruction.胆固醇和胆汁盐在胆囊动力障碍和炎症发病机制中的作用:胆囊炎不是由胆囊管阻塞引起的。
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Epidemiology of gallbladder disease: cholelithiasis and cancer.
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