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Abstract Title:Notoginsenoside R1 can inhibit the interaction between FGF1 and VEGFA to retard足细胞凋亡。
摘要来源:
bmc内克疾病。 2023年7月6日; 23(1):140。 EPUB 2023 7月6日。PMID: 37415174 37415174 JingYuan Ma, Zhang Liang, Le Zhang, Tao Liu, WenXing Fan
Article Affiliation:ChangYan Li
Abstract:BACKGROUND: Diabetic nephropathy (DN) is a chronic condition resulting from microangiopathy in a high-glucose 环境。 DN中血管损伤的评估主要集中在VEGF的活性分子上,即VEGFA和VEGF2(F2R)。 Notoginsenoside R1(NGR1),一种传统的抗炎药位血管活性。因此,识别具有血管炎症性保护的经典药物以治疗DN是一种有价值的追求。
RESULTS: According to the Swiss target prediction, the LEU32(B)血管内皮生长因子A(VEGFA)蛋白以及Lys112(a),Ser116(a)和His102(b)位点的成纤维细胞生长因子1(FGF1)蛋白的lys112(a),Ser116(a)和His102(b)位点是潜在的NG的潜在结合位点的位点R1通过氢键。此外,共免疫沉淀(COIP)结果表明VEGFA和FGF1蛋白可以彼此相互作用,而NGR1可以阻碍这种相互作用。 Furthermore, NGR1 can suppress the expression of VEGFA and FGF1 in a high-glucose environment, thereby decelerating podocyte apoptosis.
CONCLUSION: The inhibition of the interaction between FGF1 and VEGFA by NGR1 has been observed to decelerate足细胞凋亡。