[1]黄婷,程艳芳,潘铭东,等.益景汤经PI3K/AKT/eNOS信号通路拮抗高糖诱导的视网膜血管内皮细胞损伤[J].福建医药杂志,2023,45(02):99-103.
　HUANG Ting,CHENG Yanfang,PAN Mingdong,et al.Yijing Decoction inhibits retinal microvascular endothelial cell injury induced by high glucose through PI3K/AKT/eNOS signal pathway[J].FUJIAN MEDICAL JOURNAL,2023,45(02):99-103.
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益景汤经PI3K/AKT/eNOS信号通路拮抗高糖诱导的视网膜血管内皮细胞损伤()
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《福建医药杂志》[ISSN:1002-2600/CN:35-1071/R]

卷:
45
期数:
2023年02期
页码:
99-103
栏目:
基础研究
出版日期:
2023-04-15

文章信息/Info

Title:
Yijing Decoction inhibits retinal microvascular endothelial cell injury induced by high glucose through PI3K/AKT/eNOS signal pathway
文章编号:
1002-2600(2023)02-0099-05
作者:
黄婷; 程艳芳; 潘铭东1; 刘光辉1; 何建忠1; 2; 郑永征1; 3
福建中医药大学第一临床医学院（福州 350004）
Author(s):
HUANG Ting;  CHENG Yanfang;  PAN Mingdong;  LIU Guanghui;  HE Jianzhong;  ZHENG Yongzheng
First Clinical Medicine College, Fujian University of Traditional Chinese Medicine, Fuzhou, Fujian 350004, China
关键词:
益景汤; 高糖; 内皮细胞损伤; PI3K/AKT/eNOS信号通路
Keywords:
Yijing Decoction;  high glucose;  endothelial cell injury;  PI3K/AKT/eNOS signal pathway
分类号:
R587.1;R744.1
文献标志码:
A
摘要:
目的 探讨益景汤对高糖诱导大鼠视网膜微血管内皮细胞损伤的拮抗作用及机制。方法 将大鼠视网膜微血管内皮细胞随机分为5组：对照组（CG）、高糖组(HG)、低浓度益景汤组(LYG)、中浓度益景汤组(MYG)、高浓度益景汤组(HYG)。细胞生长至80%～90%时，往高糖组及益景汤组培养基中加入33 mmol/L葡萄糖培养3 d造高糖内皮细胞损伤模型，第4天按分组加入相应正常糖培养基及各浓度益景汤培养24 h。使用CCK-8试剂盒检测内皮细胞活性，Transwell法观察内皮细胞迁移，荧光聚合酶链式反应(PCR)检测细胞间紧密连接蛋白ZO-1及内皮细胞磷脂酰肌醇三羟基激酶(PI3K)、苏氨酸蛋白激酶(AKT)、内皮型一氧化氮合酶(eNOS)的信使RNA（mRNA）表达。结果 高糖条件下，大鼠视网膜微血管内皮细胞活性降低，与对照组比较，差异有统计学意义（均P<0.05）；与高糖组比较，低、中、高浓度益景汤组细胞活性均高于高糖组，差异均有统计学意义（均P<0.05）。高糖条件下，大鼠视网膜微血管内皮细胞迁移增强，与对照组比较，差异有统计学意义（P<0.05）；与高糖组比较，低、中、高浓度益景汤组细胞迁移均低于高糖组，差异均有统计学意义（均P<0.05）。高糖条件下，大鼠视网膜微血管内皮细胞间连接蛋白ZO-1及内皮细胞PI3K、AKT、eNOS的mRNA表达量均降低，与对照组比较，差异均有统计学意义（均P<0.05）；与高糖组比较，低、中、高浓度益景汤组细胞间连接蛋白ZO-1及内皮细胞PI3K、AKT、eNOS的mRNA表达量均高于高糖组，差异均有统计学意义（均P<0.05）。结论 益景汤能经PI3K/AKT/eNOS信号通路抑制高糖诱导视网膜微血管内皮细胞迁移，提高细胞活性，减轻细胞损伤。
Abstract:
Objective To investigate the protective effect and mechanism of Yijing Decoction on retinal vascular endothelial cell injury induced by high glucose in rats. Methods Rat retinal microvascular endothelial cells were randomly divided into five groups: control group (CG), high glucose group (HG), low concentration Yijing Decoction group (LYG), medium concentration Yijing Decoction group (MYG) and high concentration Yijing Decoction group (HYG). When the cells grew to 80%-90%, the high glucose endothelial cell injury model was established by adding 33 mmol/L glucose to the culture medium of high glucose group and Yijing Decoction groups for three days, and the corresponding normal glucose medium and Yijing Decoction of various concentrations were added for 24 hours on the 4th day. Endothelial cell viability was detected by CCK-8 kit, endothelial cell migration was observed by Transwell method, and the mRNA expression of intercellular connexin ZO-1 and endothelial cell PI3K, AKT and eNOS was detected by fluorescent PCR. Results Under the condition of high glucose, the activity of retinal microvascular endothelial cells in the control group was significantly lower than that in the control group (all P<0.05). The cell activity in the low, middle and high concentration Yijing Decoction groups were significantly higher than that in the high glucose group (all P<0.05). The migration of retinal microvascular endothelial cells in the high glucose group was significantly higher than that in the control group (P<0.05), and the cell migration in the low, middle and high concentration Yijing Decoction groups were significantly lower than that in the high glucose group (all P<0.05). Under the condition of high glucose, the mRNA expression of ZO-1, PI3K, AKT and eNOS in retinal microvascular endothelial cells were significantly lower than those in the control group. Compared with the high glucose group, the mRNA expression of intercellular connexin ZO-1 and endothelial cell PI3K, AKT and eNOS in the low, middle and high concentration Yijing Decoction groups were significantly higher than those in the high glucose group (all P<0.05). Conclusion Yijing Decoction can antagonize the expression of PI3K, AKT, eNOS and ZO-1mRNA in retinal microvascular endothelial cells of rats injured by high glucose, reduce endothelial cell migration, increase endothelial cell activity and reduce microvascular endothelial cell injury.

参考文献/References:

[1] Cheloni R,Gandolfi S A,Signorelli C,et al.Global prevalence of diabetic retinopathy: protocol for a systematic review and meta-analysis[J].BMJ Open,2019,9(3):e22188.
[2] Strain W D,Paldanius P M.Diabetes,cardiovascular disease and the microcirculation[J].Cardiovasc Diabetol,2018,17(1):57.
[3] 刘光辉,张云辉,郑永征,等.益景汤对糖尿病大鼠血-视网膜屏障的影响[J].中国中医眼科杂志,2021,31(12):851-855.
[4] Gao J,Ailifeire M,Wang C,et al.miR-320/VEGFA axis affects high glucose-induced metabolic memory during human umbilical vein endothelial cell dysfunction in diabetes pathology[J].Microvasc Res,2020,127:103913.
[5] 赵佳迪,高泓.参芪复方对高糖“代谢记忆”介导的人脐静脉内皮细胞的影响[J].中国临床药理学杂志,2022,38(6):532-536.
[6] Mrugacz M,Bryl A,Zorena K.Retinal vascular endothelial cell dysfunction and neuroretinal degeneration in diabetic patients[J].J Clin Med,2021,10(3):458.
[7] Wang Z,Li Y,Yao J,et al.Selenoprotein S attenuates high glucose and/or ox-LDL-induced endothelium injury by regulating Akt/mTOR signaling and autophagy[J].Int J Biochem Cell Biol,2021,141:106111.
[8] Duan M X,Zhou H,Wu Q Q,et al.Andrographolide protects against HG-induced inflammation,apoptosis,migration,and impairment of angiogenesis via PI3K/AKT-eNOS signalling in HUVECs[J].Mediators Inflamm,2019,2019:6168340.
[9] Tervonen A,Ihalainen T O,Nymark S,et al.Structural dynamics of tight junctions modulate the properties of the epithelial barrier[J].PLoS One,2019,14(4):e214876.
[10] Cong X,Kong W.Endothelial tight junctions and their regulatory signaling pathways in vascular homeostasis and disease[J].Cell Signal,2020,66:109485.
[11] 杨梦珍,汪琳.AMPK激活通过调控氧化应激修复高糖诱导的人脑微血管内皮细胞损伤[J].中国组织化学与细胞化学杂志,2020,29(1):1-7.
[12] Hamamdzic D,Fenning R S,Patel D,et al.Akt pathway is hypoactivated by synergistic actions of diabetes mellitus and hypercholesterolemia resulting in advanced coronary artery disease[J].Am J Physiol Heart Circ Physiol,2010,299(3):H699-H706.
[13] Zhang Z,Zhang D.[BF](－)[BFQ]-Epigallocatechin-3-gallate inhibits eNOS[JP] uncoupling and alleviates high glucose-induced dysfunction and apoptosis of human umbilical vein endothelial cells by PI3K/AKT/eNOS pathway[J].Diabetes Metab Syndr Obes,2020,13:2495-2504.
[14] Lin F,Yang Y,Wei S,et al.Hydrogen sulfide protects against high glucose-induced human umbilical vein endothelial cell injury through activating PI3K/Akt/eNOS pathway[J].Drug Des Devel Ther,2020,14:621-633.
[15] Ren J,Zhang S,Pan Y,et al.Diabetic retinopathy: Involved cells,biomarkers,and treatments[J].Front Pharmacol,2022,13:953691.
[16] 李剑,张文风.基于网络药理学和分子对接探讨补阳还五汤治疗糖尿病脑病的作用机制[J].世界中医药,2022,17(5):651-657.
[17] 张亚楠,张皓翔,马赟,等.基于网络药理学探究补阳还五汤治疗糖尿病肾病的作用机制[J].中国中西医结合肾病杂志,2021,22(11):985-989.
[18] 郑永征,谢茂松,刘光辉,等.加味补阳还五汤对糖尿病大鼠视网膜血管的影响[J].福建医科大学学报,2013,47(1):34-38.
[19] 郑永征,谢茂松,刘光辉,等.加味补阳还五汤对糖尿病大鼠视网膜血流动力学的影响[J].山西中医学院学报,2013,14(2):24-27.
[20] 刘光辉,刘安,郑永征,等.加味补阳还五汤对糖尿病大鼠视网膜微血管周细胞凋亡的影响[J].北京中医药大学学报,2013,36(3):178-182.

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备注/Memo

备注/Memo:
基金项目：福建省自然科学基金资助项目（2020J011037；2022J01352）
1 福建中医药大学附属人民医院 福建中医药大学中西医结合眼科研究所；2 共同通信作者，Email:37319300@qq.com；3 通信作者，Email：dandelion_zyz@163.com
更新日期/Last Update: 2023-04-15