实用肝脏病杂志 ›› 2021, Vol. 24 ›› Issue (6): 923-926.doi: 10.3969/j.issn.1672-5069.2021.06.039

• 胆石症 • 上一篇    下一篇

结石性胆囊炎患者胆囊黏膜组织Hp DNA及CagA和CCK-AR表达研究*

熊茂程, 雷艳梅, 李良敏, 李杨   

  1. 610000 成都市 成都中医药大学附属医院核医学科
  • 收稿日期:2021-05-08 发布日期:2021-11-15
  • 通讯作者: 雷艳梅,E-mail:514241827@qq.com
  • 作者简介:熊茂程,男,31岁,大学本科,初级检验师。E-mail:xiongmaocheng2@163.com
  • 基金资助:
    *四川省科技厅科技发展计划项目(编号:2020354)

Gallbladder mucosal tissue helicobacter pylori infection and its toxic gene levels in patients with gallbladder calculous cholecystitis

Xiong Maocheng, Lei Yanmei, Li Liangmin, et al   

  1. Department of Nuclear Medicine, Affiliated Hospital, Chengdu University of Traditional Chinese Medicine, Chengdu 610000, Sichuan Province, China
  • Received:2021-05-08 Published:2021-11-15

摘要: 目的 分析结石性胆囊炎患者胆囊黏膜组织幽门螺杆菌(Hp) DNA)及细胞毒素相关基因A(CagA)和胆囊收缩素-A受体(CCK-AR)基因水平变化。方法 2019年1月~2020年12月我院收治的98例行手术治疗的结石性胆囊炎患者,取胆囊粘膜组织行超微结构检查,采用PCR法检测胆囊黏膜Hp DNA及CagA和CCK-AR水平,采用盐酸滴定法检测胆囊黏膜磷脂酶A2(PLA2)活性。结果 在透射电镜下观察,发现胆囊黏膜上皮单纯性增生33例,肠型化生45例和异型增生20例;三组胆囊黏膜Hp DNA阳性率分别为30.3%、40.0%和50.0%,差异无统计学意义(P>0.05);单纯性增生组胆囊黏膜CagA mRNA相对水平和PLA2活性分别为(1.9±0.4)和(160.5±21.5)U/L,均显著低于肠型化生组【(3.3±0.6)和(170.9±20.4)U/L】或异型增生组【(5.1±0.9)和(188.9±22.3)U/L,P<0.05】,肠型化生组则显著低于异型增生组(P<0.05),而胆囊黏膜CCK-AR mRNA相对水平为(7.0±1.4),显著高于肠型化生组的(5.4±1.1)或异型增生组的【(2.9±0.6),P<0.05】,肠型化生组也显著高于异型增生组(P<0.05)。结论 Hp感染可能通过上调CagA表达和/或PLA2活性,而下调CCK-AR表达等方式,加速胆囊黏膜病变的进程,可能导致胆囊病变恶变。

关键词: 结石性胆囊炎, 幽门螺杆菌, 细胞毒素相关基因A, 胆囊收缩素-A受体, 超微结构

Abstract: Objective The aim of this study was to probe gallbladder mucosal tissue helicobacter pylori (Hp) infection and its toxic gene cytotoxin-associated gene A (CagA) and cholecystokinin-A receptor (CCK-AR) mRNA in patients with gallbladder calculous cholecystitis. Methods 98 patients with calculous cholecystitis were enrolled in our hospital between January 2019 and December 2020, and all patients underwent surgical removal of gallbladder. The Hp DNA in gallbladder mucosa was detected by polymerase chain reaction amplification, and the CagA and CCK-AR mRNA levels were measured by real-time fluorescent quantitative polymerase chain reaction. The activity of gallbladder mucosal phospholipase A2 (PLA2) was detected by hydrochloric titration. Results The transmission electron microscopy showed simple hyperplasia of gallbladder mucosal epithelium in 33 cases, intestinal metaplasia in 45 cases, and dysplasia in 20 cases; the gallbladder mucosa Hp DNA positive rates in simple hyperplasia, intestinal metaplasia and dysplasia group were 30.3%, 40.0% and 50.0%, respectively, without significant differences among them (P>0.05); the relative CagA mRNA level and the activity of PLA2 in patients with gallbladder mucosa dysplasia were(5.1±0.9) and (188.9±22.3)U/L, both significantly higher than [(1.9±0.4)和(160.5±21.5)U/L, respectively, P<0.05] in patients with simple hyperplasia of gallbladder mucosa or [(3.3±0.6) and (170.9±20.4)U/L, respectively, P<0.05] in patients with intestinal metaplasia of gallbladder mucosa, while the relative CCK-AR mRNA level was (2.9±0.6), significantly lower than [(7.0±1.4), P<0.05] in patients with simple hyperplasia of gallbladder mucosa or [(5.4±1.1), P<0.05] in patients with intestinal metaplasia of gallbladder mucosa. Conclusion Hp infection might accelerate the gallbladder mucosal lesion progression by up-regulating CagA mRNA levels and the activity of PLA2, while by down-regulating CCK-AR mRNA levels, which needs further investigation.

Key words: Calculous cholecystitis, Helicobacter pylori, Cytotoxin-associated gene A, Cholecystokinin-A receptor, Ultrastructure