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绿原酸通过Nrf2/HO-1信号通路抑制NLPR3炎性小体激活,从而减轻重症急性胰腺炎的发展。

Chlorogenic acid alleviates the development of severe acute pancreatitis by inhibiting NLPR3 Inflammasome activation via Nrf2/HO-1 signaling.

作者信息

Ye Zhen, Cheng Lin, Xuan Yujun, Yu Kui, Li Jiong, Gu Honggang

机构信息

Department of General Surgery, Longhua Hospital Shanghai University of Traditional Chinese Medicine, No. 725, Wanping South Road, Xuhui District, Shanghai 200032, China.

Department of General Surgery, Pudong Branch, Longhua Hospital Shanghai University of Traditional Chinese Medicine, Shanghai, China.

出版信息

Int Immunopharmacol. 2025 Apr 4;151:114335. doi: 10.1016/j.intimp.2025.114335. Epub 2025 Feb 22.

DOI:10.1016/j.intimp.2025.114335
PMID:39987635
Abstract

Severe acute pancreatitis (SAP), marked by profound tissue inflammation within the pancreatic tissue, is an abrupt and intense inflammation of the pancreas. Chlorogenic acid (CGA) is one of the effective pharmacological ingredients components in JinHong Tablet (JHT). The role of CGA in protecting pancreas from severe injury in pancreatitis needs to be studied. The intervention with CGA led to a significant decline in serum amylase and lipase levels in rats with SAP, concurrently mitigating the pathological impairment within the pancreatic tissue. CGA effectively diminishes the levels of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) in SAP rats by inhibiting the activation of NF-κB and the NLRP3 inflammasome. Additionally, in AR42J cells, the application of CGA was found to reduce the inflammatory response induced by caerulein. Mechanically, CGA alleviates the inflammatory response in SAP models by activating the Nrf2/HO-1 pathway. Together, CGA reduces the inflammatory response of SAP by activating the Nrf2/HO-1 pathway, thus alleviating the development of SAP. Our results provide a basis for the treatment of SAP.

摘要

重症急性胰腺炎(SAP)以胰腺组织内严重的组织炎症为特征,是胰腺的一种突发且强烈的炎症。绿原酸(CGA)是金红片(JHT)中的有效药理成分之一。CGA在胰腺炎中保护胰腺免受严重损伤的作用有待研究。用CGA干预可使SAP大鼠的血清淀粉酶和脂肪酶水平显著下降,同时减轻胰腺组织内的病理损伤。CGA通过抑制NF-κB和NLRP3炎性小体的激活,有效降低SAP大鼠体内促炎细胞因子(IL-1β、IL-6和TNF-α)的水平。此外,在AR42J细胞中,发现应用CGA可减轻雨蛙肽诱导的炎症反应。从机制上讲,CGA通过激活Nrf2/HO-1途径减轻SAP模型中的炎症反应。总之,CGA通过激活Nrf2/HO-1途径降低SAP的炎症反应,从而减轻SAP的发展。我们的结果为SAP的治疗提供了依据。

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