Tetramethylpyrazine and paeoniflorin combination(TMP-PF)inhibits angiogenesis in atherosclerosis via miR-126/VEGF/VEGFR2 signaling pathway  

作　　者：Yahui Yuan Rong Yuan Qiqi Xin Yu Miao Ying Chen Rui Gao Weihong Cong 

机构地区：[1]Laboratory of Cardiovascular Diseases,Xiyuan Hospital,China Academy of Chinese Medical Sciences,Beijing 100091,China [2]National Clinical Research Center for Chinese Medicine Cardiology,Xiyuan Hospital,China Academy of Chinese Medical Sciences,Beijing 100091,China [3]School of Health Economics and Management,Nanjing University of Chinese Medicine,Nanjing 210023,China [4]Institution of Clinical Pharmacology,Xiyuan Hospital,China Academy of Chinese Medical Sciences,Beijing 100091,China [5]Key Laboratory for Clinical Research and Evaluation of Traditional Chinese Medicine,National Medical Products Administration,Beijing 100091,China

出　　处：《Journal of Future Foods》2024年第3期280-287,共8页未来食品学报（英文）

基　　金：supported by the National Natural Science Foundation of China(82004193);CACMS Innovation Fund(CI 2021A00914);the Fundamental Research Funds for the Central Public Welfare Research Institutes(ZZ14-YQ-007).

摘　　要：Angiogenesis in atherosclerosis(AS)promotes plaque destabilization.miR-126 has a significant role in angiogenesis.Tetramethylpyrazine(TMP)and paeoniflorin(PF)have anti-atherosclerotic effects.However,the miR-126-related mechanisms of TMP and PF combination(TMP-PF)on angiogenesis in AS have not been understood.To explore the mechanism of TMP-PF on angiogenesis in AS targeting miR-126.Human umbilical vein endothelial cells(HUVECs)were assigned into the control,model,TMP-PF,TMP-PF+miR-126 inhibitor,and simvastatin groups.HUVECs were transfected with miR-126 inhibitor or negative control,incubated with oxidized low-density lipoprotein(ox-LDL)to establish AS model,and then treated with TMP-PF or simvastatin.Cell proliferation,migration,and tube formation assays are conducted,and the expression of angiogenesis-related factors were detected by enzyme-linked immunosorbent assay(ELISA)and Western blotting.The expression level of miR-126 was confirmed by polymerase chain reaction(PCR).0x-LDL promoted HUVECs proliferation,migration,and tube formation,downregulated miR-126 expression,and increased the expression of VEGF,VEGFR2,bFGF,and FGFR1.TMP-PF inhibited proliferation,migration,and tube formation,upregulated miR-126 expression and decreased the expression of VEGF,VEGFR2,bFGF,and FGFR1 in ox-LDL-induced HUVECs.However,the effects of TMP-PF on angiogenesis and the expression of miR-126,VEGF,VEGFR2,and FGFR1 were abolished by miR-126 inhibitor.TMP-PF suppressed angiogenesis in AS by regulating miR-126/VEGF/VEGFR2 pathway,which might elucidate the underlying mechanism of TMP-PF in alleviating AS.

关 键 词：ATHEROSCLEROSIS ANGIOGENESIS TETRAMETHYLPYRAZINE PAEONIFLORIN miR-126/VEGF/VEGFR2 signaling pathway 

分 类 号：R743.3[医药卫生—神经病学与精神病学]