湖南师范大学学报（医学版）
湖南師範大學學報（醫學版）
호남사범대학학보（의학판）
JOURNAL OF HUNAN NORMAL UNIVERSITY(MEDICAL SCIENCE)
2015年
2期
1-4
,共4页
张婧%张勇%刘诗炜%黄荷%杨舒婷%符晓华
張婧%張勇%劉詩煒%黃荷%楊舒婷%符曉華
장청%장용%류시위%황하%양서정%부효화
7- 二氟甲氧基 -5%4'- 二甲氧基金雀异黄素%人脐静脉内皮细胞%肿瘤坏死因子 -α%环氧化酶 -2%炎症反应
7- 二氟甲氧基 -5%4'- 二甲氧基金雀異黃素%人臍靜脈內皮細胞%腫瘤壞死因子 -α%環氧化酶 -2%炎癥反應
7- 이불갑양기 -5%4'- 이갑양기금작이황소%인제정맥내피세포%종류배사인자 -α%배양화매 -2%염증반응
7-difluoromethoxy-5,4'-dimethoxygenistein%human umbilical vein endothelial cells%tumor necrosis factor-alpha%cyclooxygenase-2%inflammation
目的：观察7-二氟甲氧基-5，4'-二甲氧基金雀异黄素（DFMG）对损伤的人脐静脉内皮细胞（HUVE-12）中环氧化酶2（cyclooxygenase-2，C0X-2）蛋白表达的影响及内皮细胞的保护作用。方法：TNF-α诱导建立人脐静脉内皮细胞（HUVE-12）损伤模型，不同浓度的 DFMG 进行干预；流式细胞术检测细胞凋亡、Western Blot 检测COX-2蛋白表达、ELISA 检测 E-选择素、单核趋化蛋白-1（Monocyte chemoattractant protein-1，MCP-1）的释放，蛋白定量分析法测定内皮细胞与单核细胞的黏附率。结果：DFMG 呈浓度依赖性阻断损伤的内皮细胞活性的下降、下调 COX-2蛋白的表达、降低内皮细胞与单核细胞的黏附率。结论：DFMG 可能通过下调 COX-2蛋白表达水平，从而减少单核细胞/内皮细胞黏附作用，减少炎症渗出，抑制炎症反应，保护血管内皮。
目的：觀察7-二氟甲氧基-5，4'-二甲氧基金雀異黃素（DFMG）對損傷的人臍靜脈內皮細胞（HUVE-12）中環氧化酶2（cyclooxygenase-2，C0X-2）蛋白錶達的影響及內皮細胞的保護作用。方法：TNF-α誘導建立人臍靜脈內皮細胞（HUVE-12）損傷模型，不同濃度的 DFMG 進行榦預；流式細胞術檢測細胞凋亡、Western Blot 檢測COX-2蛋白錶達、ELISA 檢測 E-選擇素、單覈趨化蛋白-1（Monocyte chemoattractant protein-1，MCP-1）的釋放，蛋白定量分析法測定內皮細胞與單覈細胞的黏附率。結果：DFMG 呈濃度依賴性阻斷損傷的內皮細胞活性的下降、下調 COX-2蛋白的錶達、降低內皮細胞與單覈細胞的黏附率。結論：DFMG 可能通過下調 COX-2蛋白錶達水平，從而減少單覈細胞/內皮細胞黏附作用，減少炎癥滲齣，抑製炎癥反應，保護血管內皮。
목적：관찰7-이불갑양기-5，4'-이갑양기금작이황소（DFMG）대손상적인제정맥내피세포（HUVE-12）중배양화매2（cyclooxygenase-2，C0X-2）단백표체적영향급내피세포적보호작용。방법：TNF-α유도건립인제정맥내피세포（HUVE-12）손상모형，불동농도적 DFMG 진행간예；류식세포술검측세포조망、Western Blot 검측COX-2단백표체、ELISA 검측 E-선택소、단핵추화단백-1（Monocyte chemoattractant protein-1，MCP-1）적석방，단백정량분석법측정내피세포여단핵세포적점부솔。결과：DFMG 정농도의뢰성조단손상적내피세포활성적하강、하조 COX-2단백적표체、강저내피세포여단핵세포적점부솔。결론：DFMG 가능통과하조 COX-2단백표체수평，종이감소단핵세포/내피세포점부작용，감소염증삼출，억제염증반응，보호혈관내피。
Objective To observe the effect of 7-difluoromethoxy-5, 4'- dimethoxygenistein(DFMG) on the expression of COX-2 and endothelium protection in the impaired human umbilical vein endothelial(HUVE-12) cells. Methods The model of injured HUVE-12 is established by Tumor necrosis factor(TNF-α)which was dealt with different concentrations of DFMG. The apoptosis was detected by flow cytometry using Annexin V/PI staining.The expression levels of cyclooxygenase-2 (COX-2) were detected by western blotting.The content of the fragments of E-selectin,monocyte chemoattractant protein-1 (MCP-1) was detected by the method of ELISA, the monocyte/endothelial cell adhesion was detected by protein quantitative analysis method. Results DFMG can interdict the decline of injured HUVE-12 activation, down-regulate the expression of COX-2 and an-tagonize the adhesion between endothelial cells and monocytes in a concentration dependent manner. Conclusion DFMG may antagonize TNF-α-induced inflammation in HUVE-12 cells by down-regulating the expression of COX-2 which can reduce inflammatory exudation, inhibit inflammation and protect vascular endothelium from resistant atherosclerosis.
