基于内皮细胞Ang/Tie2轴抗炎作用探讨化疗性静脉炎发病机制  被引量:2

Exploration of the pathogenesis of chemotherapeutic phlebitis based on the anti-inflammatory effect of the Ang/Tie2 axis of endothelial cells

在线阅读下载全文

作  者:王淑敏 冯玛莉[1] 吉海杰[1] WANG Shumin;FENG Mali;JI Haijie(Institute of Traditional Chinese Medicine of Shanxi Province,Shanxi,Taiyuan 030012,China)

机构地区:[1]山西省中医药研究院,山西太原030012

出  处:《中国医药科学》2023年第18期18-22,共5页China Medicine And Pharmacy

基  金:国家自然科学基金(81973672);山西省卫生健康委员会“四个一批”科技兴医创新计划(2020SYS06)。

摘  要:化疗性静脉炎一般是指静脉内长期输入浓度较高、刺激性较强的药物,导致血管内皮及周围组织存在炎性细胞浸润的一种常见并发症。受损的血管内皮细胞和炎性细胞均可产生多种炎性因子,从而激活炎症相关的信号通路,介导炎症的发展。与此相反,有一类保护性细胞因子或其他蛋白可抑制炎症的发生发展,维持血管的稳定状态,例如酪氨酸蛋白激酶-2(Tie2)。Tie2是血管生成素家族蛋白(Ang)的受体,其介导的Ang/Tie2轴调节出生后的血管生成、血管重塑、血管通透性和炎症,以维持血管的稳态。本文描述了Ang/Tie2信号传导的生物学功能,总结了Ang/Tie2信号传导对血管内皮细胞的调节作用,以此来探讨Ang/Tie2轴在化疗性静脉炎中的抗炎机制。Chemotherapeutic phlebitis generally refers to a common complication of long-term infusion of drugs with high concentration and strong stimulation into the vein,leading to inflammatory cell infiltration in the vascular endothelium and surrounding tissues.Damaged endothelial cells and inflammatory cells can produce various inflammatory factors,thereby activating inflammation-related signaling pathways and mediating the development of inflammation.On the contrary,there is a type of protective cytokines or other proteins that can inhibit the occurrence and development of inflammation,maintaining the stable state of blood vessels,such as the tyrosine-protein kinase receptor(Tie2).Tie2 is the receptor of angiopoietins(Ang),which mediates the Ang/Tie2 axis to regulate postnatal angiogenesis,vascular remodeling,vascular permeability and inflammation to maintain vascular homeostasis.This review describes the biological functions of Ang/Tie2 signal transduction and summarizes the regulatory effect of Ang Tie2 signal transduction on vascular endothelial cells,in order to explore the anti-inflammatory mechanism of Ang Tie2 axis in chemotherapeutic phlebitis.

关 键 词:化疗性静脉炎 内皮细胞 血管生成素1 血管生成素2 酪氨酸蛋白激酶-2 

分 类 号:R363.21[医药卫生—病理学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象