PDF(Pubmed)
Abstract：
BACKGROUND: Impaired interstitial cells of Cajal (ICCs) are central to the pathophysiology of acute cholecystitis (AC). Common bile duct ligation is a common model of AC, producing acute inflammatory changes and decrease in gallbladder contractility.
OBJECTIVE: To investigate the origin of slow wave (SW) in the gallbladder and the effect of ICCs on gallbladder contractions during the process of AC.
METHODS: Methylene blue (MB) with light was used to establish selective impaired ICCs gallbladder tissue. Gallbladder motility was assessed using the frequency of SW and gallbladder muscle contractility in vitro in normal control (NC), AC12h, AC24h, and AC48h groups of guinea pigs. Hematoxylin and eosin and Masson-stained gallbladder tissues were scored for inflammatory changes. ICCs pathological changes alterations were estimated using immunohistochemistry and transmission electron microscopy. The alterations of c-Kit, α-SMA, cholecystokinin A receptor (CCKAR), and connexin 43 (CX43) were assessed using Western blot.
RESULTS: Impaired ICCs muscle strips resulted in the decrease in gallbladder SW frequency and contractility. The frequency of SW and gallbladder contractility were significantly lower in the AC12h group. Compared with the NC group, the density and ultrastructure of ICCs were remarkably impaired in the AC groups, especially in the AC12h group. The protein expression levels of c-Kit were significantly decreased in the AC12h group, while CCKAR and CX43 protein expression levels were significantly decreased in the AC48h group.
CONCLUSIONS: Loss ICCs could lead to a decrease in gallbladder SW frequency and contractility. The density and ultrastructure of ICCs were clearly impaired in the early stage of AC, while CCKAR and CX43 were significantly reduced at end stage.
OBJECTIVE: To investigate the origin of slow wave (SW) in the gallbladder and the effect of ICCs on gallbladder contractions during the process of AC.
METHODS: Methylene blue (MB) with light was used to establish selective impaired ICCs gallbladder tissue. Gallbladder motility was assessed using the frequency of SW and gallbladder muscle contractility in vitro in normal control (NC), AC12h, AC24h, and AC48h groups of guinea pigs. Hematoxylin and eosin and Masson-stained gallbladder tissues were scored for inflammatory changes. ICCs pathological changes alterations were estimated using immunohistochemistry and transmission electron microscopy. The alterations of c-Kit, α-SMA, cholecystokinin A receptor (CCKAR), and connexin 43 (CX43) were assessed using Western blot.
RESULTS: Impaired ICCs muscle strips resulted in the decrease in gallbladder SW frequency and contractility. The frequency of SW and gallbladder contractility were significantly lower in the AC12h group. Compared with the NC group, the density and ultrastructure of ICCs were remarkably impaired in the AC groups, especially in the AC12h group. The protein expression levels of c-Kit were significantly decreased in the AC12h group, while CCKAR and CX43 protein expression levels were significantly decreased in the AC48h group.
CONCLUSIONS: Loss ICCs could lead to a decrease in gallbladder SW frequency and contractility. The density and ultrastructure of ICCs were clearly impaired in the early stage of AC, while CCKAR and CX43 were significantly reduced at end stage.
摘要：
背景：Cajal间质细胞受损（ICCs）是急性胆囊炎（AC）病理生理学的核心。胆总管结扎是一种常见的AC模型,产生急性炎症变化和胆囊收缩力降低。
目的：探讨AC过程中胆囊慢波(SW)的起源及ICC对胆囊收缩的影响。
方法：用亚甲基蓝（MB）与光建立选择性受损的ICC胆囊组织。使用正常对照（NC）中的SW频率和胆囊肌肉收缩力体外评估胆囊运动，AC12h,AC24h,和AC48h组豚鼠。对苏木精和伊红和Masson染色的胆囊组织进行炎症变化评分。使用免疫组织化学和透射电子显微镜估计ICC病理变化。c-Kit的改动,α-SMA,胆囊收缩素A受体（CCKAR），和连接蛋白43（CX43）使用蛋白质印迹进行评估。
结果：ICCs肌条受损导致胆囊SW频率和收缩力降低。AC12h组的SW频率和胆囊收缩力显著降低。与NC组相比，AC组ICC的密度和超微结构明显受损，特别是在AC12h组中。AC12h组c-Kit蛋白表达水平显著降低,AC48h组CCKAR和CX43蛋白表达水平显著降低。
结论：ICC丢失可能导致胆囊SW频率和收缩力降低。在AC早期，ICC的密度和超微结构明显受损，而CCKAR和CX43在终末期显著降低。
目的：探讨AC过程中胆囊慢波(SW)的起源及ICC对胆囊收缩的影响。
方法：用亚甲基蓝（MB）与光建立选择性受损的ICC胆囊组织。使用正常对照（NC）中的SW频率和胆囊肌肉收缩力体外评估胆囊运动，AC12h,AC24h,和AC48h组豚鼠。对苏木精和伊红和Masson染色的胆囊组织进行炎症变化评分。使用免疫组织化学和透射电子显微镜估计ICC病理变化。c-Kit的改动,α-SMA,胆囊收缩素A受体（CCKAR），和连接蛋白43（CX43）使用蛋白质印迹进行评估。
结果：ICCs肌条受损导致胆囊SW频率和收缩力降低。AC12h组的SW频率和胆囊收缩力显著降低。与NC组相比，AC组ICC的密度和超微结构明显受损，特别是在AC12h组中。AC12h组c-Kit蛋白表达水平显著降低,AC48h组CCKAR和CX43蛋白表达水平显著降低。
结论：ICC丢失可能导致胆囊SW频率和收缩力降低。在AC早期，ICC的密度和超微结构明显受损，而CCKAR和CX43在终末期显著降低。
