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[1]黃婷,程艷芳,潘銘東,等.益景湯經PI3K/AKT/eNOS信號通路拮抗高糖誘導的視網膜血管內皮細胞損傷[J].福建醫(yī)藥雜志,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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益景湯經PI3K/AKT/eNOS信號通路拮抗高糖誘導的視網膜血管內皮細胞損傷()
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《福建醫(yī)藥雜志》[ISSN:1002-2600/CN:35-1071/R]

卷:
45
期數(shù):
2023年02期
頁碼:
99-103
欄目:
基礎研究
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
文章編號:
1002-2600(2023)02-0099-05
作者:
黃婷程艷芳潘銘東1劉光輝1何建忠12鄭永征13
福建中醫(yī)藥大學第一臨床醫(yī)學院(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
關鍵詞:
益景湯高糖內皮細胞損傷PI3K/AKT/eNOS信號通路
Keywords:
Yijing Decoction high glucose endothelial cell injury PI3K/AKT/eNOS signal pathway
分類號:
R587.1;R744.1
文獻標志碼:
A
摘要:
目的 探討益景湯對高糖誘導大鼠視網膜微血管內皮細胞損傷的拮抗作用及機制。方法 將大鼠視網膜微血管內皮細胞隨機分為5組:對照組(CG)、高糖組(HG)、低濃度益景湯組(LYG)、中濃度益景湯組(MYG)、高濃度益景湯組(HYG)。細胞生長至80%~90%時,往高糖組及益景湯組培養(yǎng)基中加入33 mmol/L葡萄糖培養(yǎng)3 d造高糖內皮細胞損傷模型,第4天按分組加入相應正常糖培養(yǎng)基及各濃度益景湯培養(yǎng)24 h。使用CCK-8試劑盒檢測內皮細胞活性,Transwell法觀察內皮細胞遷移,熒光聚合酶鏈式反應(PCR)檢測細胞間緊密連接蛋白ZO-1及內皮細胞磷脂酰肌醇三羥基激酶(PI3K)、蘇氨酸蛋白激酶(AKT)、內皮型一氧化氮合酶(eNOS)的信使RNA(mRNA)表達。結果 高糖條件下,大鼠視網膜微血管內皮細胞活性降低,與對照組比較,差異有統(tǒng)計學意義(均P<0.05);與高糖組比較,低、中、高濃度益景湯組細胞活性均高于高糖組,差異均有統(tǒng)計學意義(均P<0.05)。高糖條件下,大鼠視網膜微血管內皮細胞遷移增強,與對照組比較,差異有統(tǒng)計學意義(P<0.05);與高糖組比較,低、中、高濃度益景湯組細胞遷移均低于高糖組,差異均有統(tǒng)計學意義(均P<0.05)。高糖條件下,大鼠視網膜微血管內皮細胞間連接蛋白ZO-1及內皮細胞PI3K、AKT、eNOS的mRNA表達量均降低,與對照組比較,差異均有統(tǒng)計學意義(均P<0.05);與高糖組比較,低、中、高濃度益景湯組細胞間連接蛋白ZO-1及內皮細胞PI3K、AKT、eNOS的mRNA表達量均高于高糖組,差異均有統(tǒng)計學意義(均P<0.05)。結論 益景湯能經PI3K/AKT/eNOS信號通路抑制高糖誘導視網膜微血管內皮細胞遷移,提高細胞活性,減輕細胞損傷。
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.

參考文獻/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] 劉光輝,張云輝,鄭永征,等.益景湯對糖尿病大鼠血-視網膜屏障的影響[J].中國中醫(yī)眼科雜志,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] 趙佳迪,高泓.參芪復方對高糖“代謝記憶”介導的人臍靜脈內皮細胞的影響[J].中國臨床藥理學雜志,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] 楊夢珍,汪琳.AMPK激活通過調控氧化應激修復高糖誘導的人腦微血管內皮細胞損傷[J].中國組織化學與細胞化學雜志,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] 李劍,張文風.基于網絡藥理學和分子對接探討補陽還五湯治療糖尿病腦病的作用機制[J].世界中醫(yī)藥,2022,17(5):651-657.
[17] 張亞楠,張皓翔,馬赟,等.基于網絡藥理學探究補陽還五湯治療糖尿病腎病的作用機制[J].中國中西醫(yī)結合腎病雜志,2021,22(11):985-989.
[18] 鄭永征,謝茂松,劉光輝,等.加味補陽還五湯對糖尿病大鼠視網膜血管的影響[J].福建醫(yī)科大學學報,2013,47(1):34-38.
[19] 鄭永征,謝茂松,劉光輝,等.加味補陽還五湯對糖尿病大鼠視網膜血流動力學的影響[J].山西中醫(yī)學院學報,2013,14(2):24-27.
[20] 劉光輝,劉安,鄭永征,等.加味補陽還五湯對糖尿病大鼠視網膜微血管周細胞凋亡的影響[J].北京中醫(yī)藥大學學報,2013,36(3):178-182.

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備注/Memo

備注/Memo:
基金項目:福建省自然科學基金資助項目(2020J011037;2022J01352)
1 福建中醫(yī)藥大學附屬人民醫(yī)院 福建中醫(yī)藥大學中西醫(yī)結合眼科研究所;2 共同通信作者,Email:[email protected];3 通信作者,Email:[email protected]
更新日期/Last Update: 2023-04-15