AKBA通过Nrf2/HO-1通路抑制巨细胞中的氧化应激来缓解实验性胰腺炎
Chenchen Yuan1, Xiaowu Dong1, Songxin Xu1
1Pancreatic Center, Department of Gastroenterology, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China; Yangzhou Key Laboratory of Pancreatic Disease, Institute of Digestive Diseases, The Affiliated Hospital of Yangzhou University, Yangzhou University, China.
International immunopharmacology
|June 26, 2023
概括
乙-11-基托-β-博斯韦利克酸 (AKBA) 通过减少巨细胞的氧化应激来预防急性胰腺炎 (AP). 这种效应通过Nrf2/HO-1通路进行介导,突出显示AKBA是AP的潜在治疗剂.
科学领域:
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
- 病理生理学 病理生理学
背景情况:
- 急性胰腺炎 (AP) 涉及氧化应激和炎症.
- 乙-11-基托-β-博斯韦利克酸 (AKBA) 具有抗氧化特性.
- 研究AKBA在AP中的治疗潜力至关重要.
研究的目的:
- 评估AKBA对急性胰腺炎的影响.
- 阐明AKBA在AP中的作用的潜在分子机制.
- 确定Nrf2/HO-1通路在AKBA的保护作用中的作用.
主要方法:
- 在使用caerulein的小鼠中引起的急性胰腺炎.
- 通过血清标志物和组织学评估AP严重程度.
- 在体外研究使用骨髓衍生的巨细胞 (BMDMs) 和流细胞计.
- 对氧化应激,ROS生成和Nrf2/HO-1通路激活的评估.
- 使用条件淘汰赛小鼠精确确定Nrf2的细胞功能.
主要成果:
- AKBA治疗减少了AP的严重程度,包括血清酶水平和胰腺损伤.
- AKBA减轻了氧化应激,并提高了Nrf2和HO-1表达的调节.
- Nrf2在巨细胞中起着主要的作用,而不是在细胞中,对AKBA的保护作用.
- AKBA抑制了M1巨细胞的两极分化,并通过Nrf2/HO-1减少了通过Nrf2/HO-1生成的ROS.
- 在特定于骨髓细胞的Nrf2缺陷模型中,AKBA的保护作用丧失了.
结论:
- 在小鼠模型中,AKBA证明了对急性胰腺炎的显著保护作用.
- 该机制涉及通过Nrf2/HO-1通路抑制巨细胞中的氧化应激.
- AKBA代表了治疗急性胰腺炎的有希望的候选药物.
相关概念视频
01:27Acute Pancreatitis I: Introduction
411
Pancreatitis is inflammation of the pancreas, an organ located behind the stomach. It can be either acute or chronic.
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
Acute pancreatitis is characterized by rapid inflammation of the pancreas, often caused by factors like gallstone blockage or excessive alcohol consumption. Chronic pancreatitis, on the other hand, is a slow, progressive inflammation that may result from long-term alcohol abuse, obstructions in the pancreatic duct, or genetic factors.
The causes of acute pancreatitis include:
411
02:26NF-κB-dependent Signaling Pathway
7.5K
The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The...
NF-κB-dependent Signaling Mechanism
The...
7.5K