TL1A抗体通过抑制活性氧产生阻止高糖诱导血管内皮细胞凋亡

Anti-TL1A-Ab preventing high glucose-induced human vascular endothelial cell apoptosis through ROS inhibition

目的:探讨TL1A抗体在高糖所致活性氧(ROS)增多及细胞凋亡中的作用。方法:将培养的人脐静脉内皮细胞分为正常对照组、正常糖+TL1A组、高糖对照组、高糖+SOD+CAT组、高糖+TL1A抗体组和高渗对照组。采用流式细胞术检测人脐静脉内皮细胞ROS生成量;Annexin V/PI荧光双染色,流式细胞仪检测细胞凋亡率。结果:与正常对照组相比,高糖对照组ROS生成量增加53%,细胞凋亡率达正常的5.8倍(P<0.01)。于正常糖培养液中加入外源性TL1A蛋白,活性氧的生成量及细胞凋亡率均明显增多,显著高于正常对照组和高糖对照组(P<0.01);在高糖培养液中加入9μg/ml TL1A抗体,活性氧生成量由(71.63±6.61)降至(50.63±4.05),细胞凋亡率由(23.70±3.20)%降至(5.07±0.47)%(P<0.01)。结论:TL1A抗体通过抑制ROS产生阻止高糖诱导血管内皮细胞凋亡。

Objective To investigate the role of anti -TLI A -Ab in the prevention of high glucose- induced ROS generation and apoptosis in human umbilical vein endothelial cells（HUVEC）. Method HUVEC were divided into six groups：normal control group,5.6 mM glucose plus TLI A group, high glucosc control group, high glucose plus SOD plus CAT group,high glucose plus anti - TL1A - Ab group and high osmotic control group. ROS generation was determined by flow cytometry,apoptosis rate of HUVEC was determined by flow cytometry with Annexin V/PI double staining. Results Exposure of HUVEC to 22.4 mM glocose for 24 h resulted in a significant increase in ROS generation and apoptosis ,compared with normal control group（ P 〈 0. 01 ）. HUVEC ROS formation and apoptosis rate significantly increased after adding exogenous TL1A to mcdia containing 5.6 mM of glucose for 24 h ,compared with normal control group and high glucose control group（ P 〈 0. 01 ）. However,high glucose - induced HUVEC ROS generation and apoptosis was significantly attenuated by 9 mg/ml anti - TL1A-Ab （ 50. 63 ±4. 05 ） vs （71.63±6.61）,（5.07±0.47）% vs （23.70±3.20）%,P〈0.01）.Conclusion Anti-TL1A-Ab preventets high glucose- induced HUVEC apoptosis through ROS inhibition.