ObjectiveTo summarize the progress and challenges in the research of gallbladder cancer organoid, and explore the possible solution strategies. MethodThe literature relevant to the researches of gallbladder cancer organoid at home and abroad in recent years was reviewed. ResultsThe research of gallbladder cancer organoid was in its infancy. The gallbladder cancer organoid was mainly constructed from surgically resected gallbladder cancer tissues. Now the research of gallbladder cancer organoid had made some progress, such as on the pathogenesis and drug screening of gallbladder cancer. ConclusionsThe study on gallbladder cancer organoid can further understand the gallbladder cancer and help to speed up the update of diagnosis and treatment plan. However, the model of gallbladder cancer organoid is facing the challenges such as low construction success rate. The experience gained from organoids research in other diseases is worthy of reference.
【摘要】 目的 探讨NF-κB在重症急性胰腺炎小鼠肠黏膜屏障功能损伤中的调控机制。 方法 36只BALB/C小鼠随机分为对照组、模型组、NF-κB干预组，每组12只。18 h后处死小鼠，比较各组的腹腔内大体改变、肠黏膜病理改变，肠道通透性的变化及血清细胞因子水平，肠上皮紧密连接蛋白occludin的表达。 结果 模型组小鼠腹腔内呈明显炎症反应，肠管水肿，肠黏膜水肿，肠道通透性显著增高，NF-κB特异性阻断剂能降低肠道损伤，改善肠黏膜水肿，上调肠上皮紧密连接蛋白occludin的表达，显著降低肠道通透性，降低细胞因子水平。 结论 NF-κB阻断剂能够通过选择性的抑制NF-κB活性，改善受损的肠屏障功能。这一作用通过上调肠上皮紧密连接蛋白occludin的水平而实现。【Abstract】 Objective To investigate the roles of NF-κB in the intestinal mucosal barrier injury in mice with severe acute pancreatitis(SAP). Methods Thirty-six BALB/C mice were randomly assigned to normal control group, SAP model group and intervention group. Eighteen hours later, pathological intestinal villus changes, intestinal permeability, serum cytokines were evaluated in all three groups. Results In SAP model group, intestinal mucosa was found to be oedematous and intestinal permeability was markedly increased. NF-κB could ameliorate intestinal injury and mucosa edema, and improve intestinal permeability by upregulating occluding expression. Conclusion NF-κB could protect the function of intestinal mucosal barrier by inhibiting NF-κB activity, which suggests that NF-κB may play an intermediating role in SAP-induced intestinal failure through upregulating occluding expression.