相关实验视频
Updated: Jan 13, 2026

09:36
Isolated Pancreatic Islet Treatment and Apoptosis Measurement
Published on: May 2, 2025
821
冷气血氧化胰岛素调节THP-1单细胞信号,独立于NF-kB
Ramona Clemen1, Wiebke Dethloff1, Kevin Arlt1
1ZIK Plasmatis, Leibniz Institute for Plasma Science and Technology (INP), a member of the Leibniz Health Technologies Research Alliance, Greifswald 17489, Germany.
Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie
|January 7, 2026
概括
使用血技术制造的氧化胰岛素变体被发现可以调节免疫细胞信号通路,包括Nrf2和NF-κB,而不会引起毒性. 这些发现表明细胞特别识别氧化胰岛素,可能会影响胰岛素耐药性和相关疾病.
科学领域:
- 生物化学 生物化学
- 免疫学 免疫学 免疫学
- 细胞生物学 细胞生物学
背景情况:
- 失调的葡萄糖平衡,氧化应激和炎症有助于胰岛素抵抗.
- 在压力期间产生的反应性氧和物种可以修改生物分子,改变细胞功能和免疫性.
- 氧化改性胰岛素 (oxIns) 变种可能会影响细胞识别和信号通路.
研究的目的:
- 研究不同oxIns变体对免疫细胞信号传递的影响.
- 探索Nrf2和NF-κB通路对oxIns.的反应中的作用.
- 评估oxIns对炎症标志物和与细胞生长相关的分子的影响.
主要方法:
- 用冷物理气体等离子体模拟炎症环境,以产生oxIns变体.
- 使用小鼠免疫细胞和人类细胞系模型 (THP-1-NF-κB记者单细胞,TK6淋巴细胞).
- 分析基因表达 (GLUT4, Nrf2, HMOX1),蛋白质信号 (Akt, Erk) 和免疫反应 (细胞大小,MHC-II,IL-18).
主要成果:
- 氧Ins变种没有毒性,但调节了GLUT4,Nrf2和HMOX1.1的基因表达.
- 氧因与Akt和Erk信号通路相关.
- 在THP-1-NF-κB细胞中观察到NF-κB信号的调节,这与细胞大小,MHC-II,IL-18分泌和Akt信号的变化有关.
结论:
- 细胞表现出对氧化胰岛素变体的特定识别.
- 氧化胰岛素可以调节参与葡萄糖平衡和炎症的关键细胞信号通路.
- 这些发现表明一种新的机制,氧化胰岛素可能会影响病理生理学,包括胰岛素抵抗.
相关概念视频
Insulin: The Receptor and Signaling Pathways
2.7K
Insulin action is mediated through a receptor tyrosine kinase, akin to the IGF-1 receptor. The number of receptors per cell varies significantly, from 40 on erythrocytes to 300,000 on adipocytes and hepatocytes. The insulin receptor consists of linked α/β subunit dimers, forming a heterotetramer glycoprotein with two extracellular α subunits and two β subunits spanning the membrane. The α subunits inhibit the inherent tyrosine kinase activity of the β subunits, but...
2.7K
Hormones Regulating Blood Glucose
6.4K
Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
In addition to accelerating glucose uptake and utilization, insulin has...
6.4K
NF-κB-dependent Signaling Pathway
9.8K
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...
9.8K
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
2.2K
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are...
Insulin and C-peptide are...
2.2K
Insulin Secretory Vesicles
6.4K
Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
6.4K
Glucagon-like Receptor Agonists
836
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
836

