Gao Lili, Zhao Hongmei, Sun Hong, Huang Ying
Department of Emergency, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University Huai'an, Jiangsu Province, China.
Department of Intensive Care Unit, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University Huai'an, Jiangsu Province, China.
Am J Blood Res. 2020 Aug 25;10(4):118-123. eCollection 2020.
Acute pancreatitis (AP) is a clinically common inflammatory disease, NF-κB activation and the secretion of pro-inflammatory mediators have been considered as the main events of AP. According to reports, TAB3 is essential for NF-κB activation and participates in inflammatory responses. In this study, we used caerulein to establish an AP rat model and cell model. The expression of TAB3 was measured both in control group and AP group by Western blot and Immunohistochemistry. We firstly found the expression of TAB3 was significantly increased in caerulein-induced AP rat and cell model compared with control group, especially at 8 h. Furthermore, the increasing expression of TAB3 in AP group was also accompanied by increased levels of pro-inflammatory mediators (TNF-α, IL-6 and LDH). In addition, the decreasing expression of TAB3 in TAB3-siRNA transfected AP AR42J cells was accompanied by reduced levels of pro-inflammatory cytokines and inhibited the production of p-P65. These findings suggested that TAB3 may accelerate the inflammatory responses of AP through NF-κB activation.
急性胰腺炎（AP）是一种临床常见的炎症性疾病，核因子κB（NF-κB）激活及促炎介质分泌被认为是AP的主要发病机制。据报道，TAB3对NF-κB激活至关重要，并参与炎症反应。本研究中，我们使用雨蛙肽建立AP大鼠模型和细胞模型。通过蛋白质免疫印迹法和免疫组织化学法检测对照组和AP组中TAB3的表达。我们首次发现，与对照组相比，雨蛙肽诱导的AP大鼠和细胞模型中TAB3的表达显著增加，尤其是在8小时时。此外，AP组中TAB3表达的增加还伴随着促炎介质（TNF-α、IL-6和乳酸脱氢酶）水平的升高。此外，在转染TAB3-siRNA的AP AR42J细胞中，TAB3表达的降低伴随着促炎细胞因子水平的降低，并抑制了p-P65的产生。这些结果表明，TAB3可能通过激活NF-κB加速AP的炎症反应。
