BackgroundDiabetic nephropathy (DN) is a chronic condition resulting from microangiopathy in a high-glucose environment. The evaluation of vascular injury in DN has primarily focused on active molecules of VEGF, namely VEGFA and VEGF2(F2R). Notoginsenoside R1 (NGR1), a traditional anti-inflammatory medication, exhibits vascular activity. Therefore, identifying classical drugs with vascular inflammatory protection for the treatment of DN is a valuable pursuit.MethodsThe "Limma" method was employed to analyze the glomerular transcriptome data, while the Spearman algorithm for Swiss target prediction was utilized to analyze the drug targets of NGR1. The molecular docking technique was employed to investigate the relationship between vascular active drug targets, and the COIP experiment was conducted to verify the interaction between fibroblast growth factor 1 (FGF1) and VEGFA in relation to NGR1 and drug targets.ResultsAccording to the Swiss target prediction, the LEU32(b) site of the Vascular Endothelial Growth Factor A (VEGFA) protein, as well as the Lys112(a), SER116(a), and HIS102(b) sites of the Fibroblast Growth Factor 1 (FGF1) protein, are potential binding sites for NGR1 through hydrogen bonding. Additionally, the Co-immunoprecipitation (COIP) results suggest that VEGFA and FGF1 proteins can interact with each other, and NGR1 can impede this interaction. Furthermore, NGR1 can suppress the expression of VEGFA and FGF1 in a high-glucose environment, thereby decelerating podocyte apoptosis.ConclusionThe inhibition of the interaction between FGF1 and VEGFA by NGR1 has been observed to decelerate podocyte apoptosis.
基金：
This work was supported by a grant from the National Natural Science
Foundation of China (Project Number: 82160142), the Outstanding-Youth
Cultivation Project for Union Foundation of Yunnan Applied Basic Research
Projects (Project Number: 202201AY070001-044), and the Reserve Talents
Project for Young and Middle-aged Academic and Technical Leaders of
Yunnan Province (Project Number: 202205AC160062). The Scientific Research
Fund of the Department of Education of Yunnan Province(Project Number:
2023Y0809). The funding body played no role in the design of the study and
collection, analysis, interpretation of data, and in writing the manuscript.
第一作者机构：[1]Kunming Med Univ, Affiliated Hosp 1, Dept Nephrol, 295, Xichang Rd, Kunming 650032, Yunnan, Peoples R China
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推荐引用方式(GB/T 7714)：
Li ChangYan,Zhong HuaChen,Ma JingYuan,et al.Notoginsenoside R1 can inhibit the interaction between FGF1 and VEGFA to retard podocyte apoptosis[J].BMC ENDOCRINE DISORDERS.2023,23(1):doi:10.1186/s12902-023-01402-6.
APA：
Li, ChangYan,Zhong, HuaChen,Ma, JingYuan,Liang, Zhang,Zhang, Le...&Fan, WenXing.(2023).Notoginsenoside R1 can inhibit the interaction between FGF1 and VEGFA to retard podocyte apoptosis.BMC ENDOCRINE DISORDERS,23,(1)
MLA：
Li, ChangYan,et al."Notoginsenoside R1 can inhibit the interaction between FGF1 and VEGFA to retard podocyte apoptosis".BMC ENDOCRINE DISORDERS 23..1(2023)
