CAJ | 학술논문

目的：评价银杏内酯B对高糖诱导内皮细胞TLR4表达的影响以及分子机制。方法使用人原代脐静脉内皮细胞，用高糖刺激内皮细胞，用Western blot分析TLR4、炎症蛋白表达以及Akt 磷酸化。免疫荧光检测NF-κB核转位。结果高糖（30 mmol·L－1）刺激内皮细胞TLR4和PAF受体表达明显增加，PAF 受体抑制剂银杏内酯B （0.6 g · L－1）和CV3988（30μmol·L－1）分别抑制了TLR4及PAF受体表达。银杏内酯B有效地抑制了高糖刺激内皮细胞ICAM-1、VCAM-1表达。分子机制的研究表明，银杏内酯B明显抑制了高糖诱导的Akt磷酸化，以及NF-κB p65的核转位。结论高糖刺激内皮细胞TLR4和PAF受体表达增高，银杏内酯B能够抑制高糖刺激TLR4、PAF受体和炎症蛋白表达，分子机制与抑制Akt磷酸化以及NF-κB活化相关。
목적：평개은행내지B대고당유도내피세포TLR4표체적영향이급분자궤제。방법사용인원대제정맥내피세포，용고당자격내피세포，용Western blot분석TLR4、염증단백표체이급Akt 린산화。면역형광검측NF-κB핵전위。결과고당（30 mmol·L－1）자격내피세포TLR4화PAF수체표체명현증가，PAF 수체억제제은행내지B （0.6 g · L－1）화CV3988（30μmol·L－1）분별억제료TLR4급PAF수체표체。은행내지B유효지억제료고당자격내피세포ICAM-1、VCAM-1표체。분자궤제적연구표명，은행내지B명현억제료고당유도적Akt린산화，이급NF-κB p65적핵전위。결론고당자격내피세포TLR4화PAF수체표체증고，은행내지B능구억제고당자격TLR4、PAF수체화염증단백표체，분자궤제여억제Akt린산화이급NF-κB활화상관。
Aim To investigate the effect of ginkgolide B on TLR4 expression in glucose-treated endothelial cells.Methods Human umbilical vein endothelial cells (HUVECs)were stimulated by high concentra-tion of glucose.TLR4,inflammatory protein expression and Akt phosphorylation were analyzed by Western blot.Transcription factor NF-κB nuclear translocation was analyzed by immunofluorescence.Results The expression of TLR4 and PAF receptor was increased in high glucose-treated HUVECs. In contrast, both ginkgolide B and CV3988 dose-dependently decreased TLR4 and PAF receptor expression in high glucose-treated cells,respectively.Ginkgolide B decreased in-flammatory protein ICAM-1 ,VCAM-1 expression.Mo-reover,ginkgolide B potently abolished Akt phospho-rylation and NF-κB p65 nuclear translocation.Conclu-sion Ginkgolide B can reduce TLR4,PAF receptor, ICAM-1 and VCAM-1 expression in high dose of glu-cose-treated HUVECs,the mechanism might be linked to inhibition of Akt phosphorylation and NF-κB activa-tion.