【摘要】 目的 研究刺槐素（ACA）对高糖/高脂（HG/HF,44/1.0 mmol/L）应激所致的血管内皮功能失调的保护作用及其机制。方法 采用HG/HF应激诱导血管内皮细胞功能失调模型，采用细胞计数试剂盒8(CCK8)法、细胞划伤损伤实验、流式细胞术、分光光度法，从修复愈合、细胞凋亡、ET-1和NO水平等方面，探究ACA对HG/HF应激下的血管内皮细胞功能失调的保护与修复作用，并通过过氧化物酶体增殖物激活受体γ/核因子κB (PPARγ/NF-κB)信号通路抑制剂（T0070907）干预，考察ACA对HG/HF应激诱导血管内皮功能失调的保护与修复作用与PPARγ/NF-κB通路的关系。结果 ACA在小于等于40μmol/L细胞存活率大于80%。HG/HF造成HUVECs细胞失调后，加入ACA(40μmol/L)，人体脐静脉内皮细胞（HUVECs）细胞修复愈合能力显著提高，HUVECs细胞凋亡明显减少，ET-1含量减少，NO含量增加，证实ACA具有改善HG/HF应激诱导HUVECs细胞功能失调的作用。qRT-PCR结果显示PPARγ/NF-κB信号通路的mRNA表达上调，通过T0070907干预，ACA的改善作用也被逆转，进一步证实ACA是通过激活PPARγ/NF-κB发挥改善HG/HF应激造成的血管内皮细胞功能失调的作用。结论 ACA通过激活PPARγ/NF-κB通路达到改善HG/HF应激诱导下的HUVECs功能失调的目的。更多还原

【Abstract】 Objective To investigate the protective effect of acacetin(ACA) on vascular endothelial dysfunction caused by HG/HF(44/1.0 mmol/L) stress and its related mechanism. Methods The endothelial cell dysfunction model was established by HG/HF stress. CCK8 method, cell scratch injury test, flow cytometry and spectrophotometry were used, the protective and repairing effects of ACA on endothelial cell dysfunction under HG/HF stress were explored from the aspects of healing and repair, apoptosis, ET-1 and NO levels, etc. By PPARγ/NF-κB pathway inhibitors(T0070907) intervention to investigate the relationship between the protective and repair effects of ACA on HG/HF stress-induced vascular endothelial dysfunction and the PPAR γ/NF-κB pathway. Results ACA had a survival rate of more than 80% in cells less than or equal to 40 μmol/L. When HG/HF stressed HUVECs were added with ACA(40 μmol/L), the healing and repair displacement of cells was significantly improved; cell apoptosis decreased significantly; the content of ET-1 decreased and the content of NO increased. These results confirmed that ACA has the effect of improving the dysfunction of HUVECs cells induced by HG/HF stress. The mRNA expression of PPARγ/NF-κB signaling pathway was up-regulated by qRT-PCR. The improvement effect of ACA was also reversed by the T0070907 intervention, which further confirm that ACA can improve the function of endothelial cells induced by HG/HF stress by activating PPARγ/NF-κB. Conclusion ACA can improve the function of HUVECs under HG/HF stress by activating PPARγ/NF-κB pathway.更多还原