基础医学与临床 ›› 2025, Vol. 45 ›› Issue (2): 203-209.doi: 10.16352/j.issn.1001-6325.2025.02.0203

• 研究论文 • 上一篇    下一篇

乌司他丁联合生长抑素减轻急性胰腺炎大鼠肠道损伤

靳高超1*, 邢盼盼2, 王玉3, 刘波3   

  1. 邢台市人民医院 1.胰胆外科;
    2.消化内科;
    3.重症医学科,河北 邢台 054000
  • 收稿日期:2024-05-13 修回日期:2024-07-19 出版日期:2025-02-05 发布日期:2025-01-17
  • 通讯作者: *jiaxiayv36991@163.com
  • 基金资助:
    2023年邢台市市级科技计划自筹经费项目(2023ZC062)

Combination of ulinastatin and somatostatin attenuates intestinal injury in rats with acute pancreatitis

JIN Gaochao1*, XING Panpan2, WANG Yu3, LIU Bo3   

  1. 1. Department of Pancreaticobiliary Surgery;
    2. Department of Gastroenterology;
    3. Department of Critical Care Medicine, Xingtai People's Hospital, Xingtai 054000, China
  • Received:2024-05-13 Revised:2024-07-19 Online:2025-02-05 Published:2025-01-17
  • Contact: *jiaxiayv36991@163.com

摘要: 目的 探讨乌司他丁(UTI)与生长抑素(SOM)对急性胰腺炎(AP)大鼠肠道损伤的影响及可能的作用机制。方法 将大鼠随机分为假手术(sham)组、AP组、UTI组、UIT+SOM组和UIT+SOM+JAK2激活剂(CA1)组,分别建立AP大鼠模型立,15只/组。结束给药12 h后,检测大鼠肠道通透性以及血清生化指标、炎性因子水平;苏木精-伊红(HE)染色观察胰腺和肠道组织的病理变化;TUNEL法检测肠道组织细胞凋亡;Western blot检测Janus激酶2(JAK2)信号转导与转录激活因子3(STAT3)信号通路蛋白表达。结果 与假手术组比较,AP组大鼠胰腺组织炎性细胞浸润、水肿和出血明显,肠组织中肠黏膜出现炎性细胞浸润、绒毛不规则、肠上皮细胞脱落和坏死,肠道通透性、血清淀粉酶(AMY)和脂肪酶(LIPA)活性、二胺氧化酶(DAO)活性、肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)水平、胰腺和肠道病理组织学评分、肠组织细胞凋亡率及p-JAK2/JAK2、p-STAT3/STAT3比值均升高(P<0.05);与AP组比较,UTI组、UIT+SOM组大鼠胰腺和肠道组织损伤减轻,炎性细胞浸润减少,肠道通透性、血清AMY、LIPA活性、DAO活性、TNF-α、IL-6水平、胰腺和肠道病理组织学评分、肠组织细胞凋亡率及p-JAK2/JAK2、p-STAT3/STAT3比值均降低(P<0.05);UIT+SOM+CA1组大鼠胰腺和肠道组织损伤加重,上述指标趋势均与UIT+SOM组相反(P<0.05)。结论 UTI联合SOM可减轻AP大鼠的肠道损伤,可能与抑制JAK2/STAT3信号通路有关。

关键词: 乌司他丁, 生长抑素, 急性胰腺炎, 肠道损伤, Janus激酶2/信号转导与转录激活因子3信号通路(JAK2/STAT3)

Abstract: Objective To investigate the effects of ulinastatin (UTI) combined with somatostatin (SOM) on intestinal damage in acute pancreatitis (AP) rats and the possible mechanisms of action. Methods The rats were randomly divided into sham-operated (sham) group, AP group, UTI group, UIT+SOM group and UIT+SOM+JAK2 activator (CA1) group, 15 rats/group, respectively. Twelve hours after administration, the intestinal permeability, serum biochemical indicators, and inflammatory factor of rats were detected. HE staining was applied to observe the pathological changes in pancreatic and intestinal tissues. TUNEL method was applied to detect apoptosis in intestinal tissue. Western blot was applied to detect the expression of JAK2/STAT3 signaling pathway proteins. Results Compared with the sham group, the pancreatic tissue of rats in the AP group showed obvious inflammatory cell infiltration, edema and bleeding, while the intestinal mucosa showed inflammatory cell infiltration, irregular villi, shedding and necrosis of intestinal epithelial cells in the intestinal tissue. The intestinal permeability, serum amylase (AMY), lipase(LIPA) activities, diamine oxidase (DAO) activities, tumor necrosis factor α(TNF-α), interleukin-6(IL-6) level, pancreatic and intestinal histopathological scores, intestinal tissue cell apoptosis rate, and p-JAK2/JAK2, p-STAT3/STAT3 ratio all significantly increased (P<0.05). Compared with the AP group, the pancreatic and intestinal tissue injury of rats in the UTI group and UIT+SOM group was reduced, and inflammatory cell infiltration was reduced. The intestinal permeability, serum AMY, LIPA activities, DAO activities, TNF-α, IL-6 level, pancreatic and intestinal histopathological scores, intestinal tissue cell apoptosis rate and p-JAK2/JAK2, p-STAT3/STAT3 ratio were all decreased (P<0.05). The pancreatic and intestinal tissue injury of rats in the UIT+SOM+CA1 group were more severe, and the trends of the above indicators were opposite to those found in UIT+SOM group (P<0.05). Conclusions The combination of UTI and SOM attenuated intestinal injury in AP rats, and potential mechanism may involve in the inhibition of the JAK2/STAT3 signaling pathway.

Key words: ulinastatin, somatostatin, acute pancreatitis, intestinal injury, JAK2/STAT3

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