急性胆囊炎通过减少mRNA合成降低猪胆囊中Cajal间质细胞数量。
Acute Cholecystitis Reduces Interstitial Cells of Cajal in Porcine Gallbladder Through Decreased mRNA Synthesis.
作者信息
Huang Zhen-Peng, Qiu Hu, Yu Bao-Ping
机构信息
Teaching and Research Section of Internal Medicine, College of Clinical Medicine, Xi'an Medical University, Xi'an, China.
Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan, China.
出版信息
Cell Physiol Biochem. 2018;47(2):535-544. doi: 10.1159/000489987. Epub 2018 May 22.
BACKGROUND/AIMS: Acute cholecystitis is a common gastrointestinal disorder, often characterized by acute cholecystitis with gallbladder motility disorder. Interstitial cells of Cajal (ICCs) are the pacemaker cells of gut motility in the gastrointestinal tract. Disruption of ICC function is related to motility disorders. The aim of this study was to explore the cellular and molecular mechanisms of ICCs in acute cholecystitis and after the resolution of acute inflammation.
MATERIALS AND METHODS
Fifty adult guinea pigs were randomly divided into five groups: a sham-administered group (control group); two groups that were intraperitoneally administered an anti-polyclonal neutrophil (PMN) antibody 24 h before common bile duct ligation (CBDL); and two groups of guinea pigs that were subjected to CBDL without receiving the PMN antibody. Guinea pigs that underwent CBDL were held for 24 h or 48 h after surgery before being subjected to laparotomy and cholecystectomy. Immunohistochemistry, TUNEL assays, western blotting, and real-time PCR were performed to determine ICC morphology and density, to detect ICC apoptosis, and to examine stem cell factor (SCF) and c-kit protein expression and SCF and c-kit mRNA levels, respectively.
RESULTS
Both hematoxylin-eosin staining and histological inflammation scores in the PMN groups were lower than those in the control groups (P < 0.01). No differences were observed in ICC morphology between groups. During acute cholecystitis, ICCs numbers were reduced. Conversely, the density of ICCs increased after inflammation was relieved (P < 0.01). In addition, SCF and c-kit protein and mRNA expression levels decreased during acute cholecystitis (P < 0.05) and increased after inflammation was relieved (P < 0.05). Furthermore, ICC apoptosis increased during acute cholecystitis and decreased after resolution of acute cholecystitis (P < 0.01).
CONCLUSIONS
In acute cholecystitis, ICC injury may be related to gallbladder motility disorder.
背景/目的：急性胆囊炎是一种常见的胃肠道疾病，常表现为伴有胆囊动力障碍的急性胆囊炎。 Cajal间质细胞（ICC）是胃肠道中肠道运动的起搏细胞。 ICC功能的破坏与动力障碍有关。本研究的目的是探讨ICC在急性胆囊炎及急性炎症消退后的细胞和分子机制。
材料与方法
50只成年豚鼠随机分为五组：假手术组（对照组）；两组在胆总管结扎（CBDL）前24小时腹腔注射抗多克隆中性粒细胞（PMN）抗体；两组豚鼠接受CBDL但未接受PMN抗体。接受CBDL的豚鼠在手术后24小时或48小时进行剖腹术和胆囊切除术。进行免疫组织化学、TUNEL检测、蛋白质印迹和实时PCR，以确定ICC形态和密度，检测ICC凋亡，并分别检测干细胞因子（SCF）和c-kit蛋白表达以及SCF和c-kit mRNA水平。
结果
PMN组的苏木精-伊红染色和组织学炎症评分均低于对照组（P < 0.01）。各组间ICC形态未观察到差异。在急性胆囊炎期间，ICC数量减少。相反，炎症消退后ICC密度增加（P < 0.01）。此外，SCF和c-kit蛋白及mRNA表达水平在急性胆囊炎期间降低（P < 0.05），炎症消退后升高（P < 0.05）。此外，ICC凋亡在急性胆囊炎期间增加，在急性胆囊炎消退后减少（P < 0.01）。
结论
在急性胆囊炎中，ICC损伤可能与胆囊动力障碍有关。
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