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依达拉奉通过核因子-κB 信号通路保护急性胰腺炎小鼠的胰腺和肠道损伤。

Edaravone Protects against Pancreatic and Intestinal Injury after Acute Pancreatitis via Nuclear Factor-κB Signaling in Mice.

机构信息

Department of Anesthesiology, The First Affiliated Hospital of Wenzhou Medical University.

出版信息

Biol Pharm Bull. 2020;43(3):509-515. doi: 10.1248/bpb.b19-00944.

DOI:10.1248/bpb.b19-00944
PMID:32115510
Abstract

Acute pancreatitis (AP) is one kind of acute surgical abdominal disease in the world. It causes intestinal damage with subsequent bacterial migration, endotoxemia and secondary pancreatic infections. In this investigation, we determined that edaravone (EDA) reduces pancreatic and intestinal injury after AP in mice. This was demonstrated by a reduction in histological score, apoptosis, interleukin (IL)-6, IL-1β and tumor necrosis factor (TNF)-α, along with obstructing activation of Toll-like receptor 4 (TLR4) and nuclear factor-κB (NFκB). Our study results suggested that EDA exerts its protective effects against pancreatic and intestinal injury after AP via regulation of the TLR4/NFκB pathway. Our findings provide the basis for EDA to treat AP-induced pancreatic and intestinal injury, even might develop as a potential therapy for other inflammatory diseases.

摘要

急性胰腺炎(AP)是世界范围内的一种急性外科腹部疾病。它会导致肠道损伤,随后发生细菌迁移、内毒素血症和继发性胰腺感染。在这项研究中,我们确定了依达拉奉(EDA)可减轻 AP 小鼠的胰腺和肠道损伤。这表现在组织学评分、细胞凋亡、白细胞介素(IL)-6、IL-1β和肿瘤坏死因子(TNF)-α的降低,同时还阻断了 Toll 样受体 4(TLR4)和核因子-κB(NFκB)的激活。我们的研究结果表明,EDA 通过调节 TLR4/NFκB 通路对 AP 后胰腺和肠道损伤发挥保护作用。我们的研究结果为 EDA 治疗 AP 诱导的胰腺和肠道损伤提供了依据,甚至可能成为治疗其他炎症性疾病的一种有潜力的疗法。

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