Inhibition of TRAF6 improves hyperlipidemic acute pancreatitis by alleviating pyroptosis in vitro and in vivo rat models.
Inhibition of TRAF6 improves hyperlipidemic acute pancreatitis by alleviating pyroptosis in vitro and in vivo rat models.
复制标题
抑制TRAF6通过减轻体外和体内大鼠模型中的焦亡来改善高血压性急性胰腺炎。
DOI：
10.1186/s13062-023-00380-y
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发表时间：
2023-05-10
期刊：
影响因子：
5.5
通讯作者：
中科院分区：
文献类型：
--
作者：
高甘油三酯血症（HTG）是急性胰腺炎（AP）的常见原因之一。高脂血症性急性胰腺炎（HTG-AP）由于其严重程度更高且进展迅速，因此与较高的死亡率相关。本研究的目的是探讨肿瘤坏死因子受体相关因子6（TRAF6）参与HTG-AP过程中细胞焦亡的机制。通过体外棕榈酸处理和体内高脂肪饮食模拟 HTG 环境。使用Cerrulein建立HTG-AP模型，然后对TRAF6进行遗传和药理抑制。评估了 HTG-AP 中焦亡激活、炎症反应以及 TRAF6 与焦亡之间的相互作用。在HTG-AP模型中，HTG被发现会加重胰腺炎的发展，并伴有细胞焦亡增加和炎症反应增强。从机制上讲，TRAF6 下调减少了雨蛙素诱导的 HTG-AP 中细胞焦亡的激活。总的来说，抑制 TRAF6 可通过减轻焦亡来改善 HTG-AP 和相关炎症。
Hypertriglyceridemia (HTG) is one of the common causes of acute pancreatitis (AP). Hyperlipidemic acute pancreatitis (HTG-AP) is associated with higher mortality owing to its tendency for greater severity and rapid progression. The purpose of this study was to explore the mechanism of involvement of tumor necrosis factor receptor-related factor 6 (TRAF6) in pyroptosis during HTG-AP. The HTG environment was simulated with palmitic acid treatment in vitro and a high-fat diet in vivo. Cerulein was used to establish the HTG-AP model, followed by genetic and pharmacological inhibition of TRAF6. Pyroptosis activation, inflammatory reaction, and the interaction between TRAF6 and pyroptosis in HTG-AP were assessed. HTG was found to aggravate the development of pancreatitis, accompanied by increased pyroptosis and enhanced inflammatory response in HTG-AP models. Mechanistically, TRAF6 downregulation decreased the activation of pyroptosis in cerulein-induced HTG-AP. Collectively, inhibition of TRAF6 improved HTG-AP and the associated inflammation by alleviating pyroptosis.
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