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 探討NF-κB在重癥急性胰腺炎小鼠腸黏膜屏障功能損傷中的調控機制。 方法 36只BALB/C小鼠隨機分為對照組、模型組、NF-κB干預組，每組12只。18 h后處死小鼠，比較各組的腹腔內大體改變、腸黏膜病理改變，腸道通透性的變化及血清細胞因子水平，腸上皮緊密連接蛋白occludin的表達。 結果 模型組小鼠腹腔內呈明顯炎癥反應，腸管水腫，腸黏膜水腫，腸道通透性顯著增高，NF-κB特異性阻斷劑能降低腸道損傷，改善腸黏膜水腫，上調腸上皮緊密連接蛋白occludin的表達，顯著降低腸道通透性，降低細胞因子水平。 結論 NF-κB阻斷劑能夠通過選擇性的抑制NF-κB活性，改善受損的腸屏障功能。這一作用通過上調腸上皮緊密連接蛋白occludin的水平而實現。【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.