卡塔尔波尔通过抑制加列-3来阻止由高级糖化终产品诱导的淋巴细胞血管生成
Wei-Xiang Sun1,2,3,4, Yu-Yan Gao3,4, Ying Cao5
1Jiangsu Key Laboratory for High-Tech Research and Development of Veterinary Biopharmaceuticals, Jiangsu Agri-animal Husbandry Vocational College, Taizhou, 225300, China.
Current medical science
|July 22, 2023
概括
卡塔尔波尔是一种天然化合物,通过向加勒-3来抑制血管生成和巨细胞的增殖,从而防止糖尿病病的进展. 这项研究强调了catalpolpol.
科学领域:
- 糖尿病病 (DN) 研究研究
- 内皮细胞生物学 内皮细胞生物学
- 巨细胞免疫学
背景情况:
- 早期糖尿病病 (DN) 的特征是异常的淋巴细胞内皮细胞 (GEC) 血管生成和巨细胞透.
- 加勒-3通过与先进的糖化终产物 (AGEs) 相互作用,在DN病变发生过程中发挥关键作用.
- 卡塔尔波尔 (Catalpol) 来自Rehmannia glutinosa,显示出减轻糖尿病中血管炎症和内皮损伤的潜力.
研究的目的:
- 调查卡塔波尔是否可以抑制AGE诱导的血管生成和炎症.
- 阐明加勒-3在卡塔波尔对GEC和巨细胞的影响中的作用.
- 评估catalpol在糖尿病病的小鼠模型中的治疗潜力.
主要方法:
- 使用老鼠GEC (mGEC) 和RAW 264.7巨细胞治疗AGE和catalpol的体外研究.
- 评估细胞增殖,细胞因子水平 (VEGFA,Ang-1,Ang-2,Tie-2),以及蛋白质表达 (黄质素-3,HIF-1α,VEGFR1,VEGFR2).
- 在体内研究中,使用与catalpol或galectin-3抑制剂治疗的小鼠DN模型,然后进行组织学分析.
主要成果:
- 卡塔波尔抑制了AGEs诱导的mGEC和巨细胞的扩散,并减少了亲血管性因素.
- 在mGEC和巨细胞中,Catalpol抑制了AGEs诱导的加列-3,HIF-1α,VEGFR1和VEGFR2的表达.
- 在体内,catalpol显著减少了糖尿病大鼠的损伤,巨细胞透,原积累和血管生成.
结论:
- 卡塔尔波尔通过抑制加勒-3有效地防止GEC血管生成和巨细胞的增殖.
- 卡塔尔波尔证明了对糖尿病诱导的损伤的保护作用.
- 卡塔尔波尔代表了治疗糖尿病病的潜在治疗剂.
相关概念视频
01:09GPCRs Regulate Adenylyl Cylase Activity
5.7K
Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of...
5.7K
01:05Proteoglycans
3.9K
Glycans, a class of complex heterogeneous molecules, can be covalently attached to proteins to form glycosylated proteins that regulate various physiological and pathological processes. Glycosylated proteins or glycoproteins comprise N-linked and O-linked oligosaccharides. O-glycosylation is the most common type of protein glycosylation. Here, glycans attach to the oxygen atom of the hydroxyl groups of Serine or Threonine residues. O-linked glycosylation occurs later in protein processing,...
3.9K
01:25cAMP-dependent Protein Kinase Pathways
6.4K
Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
6.4K
01:12GPCR Desensitization
6.1K
G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
6.1K
01:23Dipeptidyl Peptidase 4 Inhibitors
213
Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
213