王钦汶, 戴新新, 项想, 宿树兰, 郭建明, 朱悦, 钱大玮, 段金廒. 丹酚酸和丹参酮干预糖尿病肾病的分子机制研究进展J. 药学学报, 2019,54(8): 1356-1363. doi: 10.16438/j.0513-4870.2018-1044
引用本文: 王钦汶, 戴新新, 项想, 宿树兰, 郭建明, 朱悦, 钱大玮, 段金廒. 丹酚酸和丹参酮干预糖尿病肾病的分子机制研究进展J. 药学学报, 2019,54(8): 1356-1363. doi: 10.16438/j.0513-4870.2018-1044
WANG Qin-wen, DAI Xin-xin, XIANG Xiang, SU Shu-lan, GUO Jian-ming, ZHU Yue, QIAN Da-wei, DUAN Jin-ao. Advances in the molecular mechanism of salvianolic acid and tanshinone for intervention of diabetic kidney diseaseJ. Acta Pharmaceutica Sinica, 2019,54(8): 1356-1363. doi: 10.16438/j.0513-4870.2018-1044
Citation: WANG Qin-wen, DAI Xin-xin, XIANG Xiang, SU Shu-lan, GUO Jian-ming, ZHU Yue, QIAN Da-wei, DUAN Jin-ao. Advances in the molecular mechanism of salvianolic acid and tanshinone for intervention of diabetic kidney diseaseJ. Acta Pharmaceutica Sinica, 2019,54(8): 1356-1363. doi: 10.16438/j.0513-4870.2018-1044

丹酚酸和丹参酮干预糖尿病肾病的分子机制研究进展

Advances in the molecular mechanism of salvianolic acid and tanshinone for intervention of diabetic kidney disease

  • 摘要: 糖尿病肾病(diabetic kidney disease,DKD)是糖尿病患者最为严重的微血管并发症,也是终末期肾病的主要原因。由于代谢和血流动力学等因素之间的相互作用,激活了导致糖尿病肾脏损伤的常见途径。研究表明,丹参酚酸可通过调节肾小管间质激活素A、转化生长因子-β1和单核细胞趋化蛋白-1来减轻肾纤维化,缓解糖尿病引起的肾损伤;还可通过对蛋白激酶ERK1/2蛋白表达的影响,参与肾小球细胞外基质的重新构建,对糖尿病肾脏具有较好的保护作用。丹参酮可抑制氧化应激介导葡萄糖诱导的肾损伤、抑制蛋白酪氨酸磷酸酶1B(protein-tyrosinephosphatase 1B,PTP1B)活性的表达、改善2型糖尿病患者中胰岛β细胞分泌功能;可通过阻断TGF-β/Smad和NF-κB信号通路、Wnt/β-catenin信号通路,减轻糖尿病肾病的肾间质纤维化。提示丹参酚酸和丹参酮类成分具有明确的防治糖尿病肾病的作用,为丹参酚酸、丹参酮类成分的深入研究与开发提供科学依据和重要支撑。

     

    Abstract: Diabetic kidney disease (DKD) is one of the most serious microvascular complications in diabetic patients, and is the leading cause of end-stage renal disease. The interaction between metabolic and hemodynamic factors leads to activation of the common pathways of diabetic kidney injury. Studies have shown that salvianolic acid can alleviate renal fibrosis and renal injury caused by diabetes by regulating renal tubular interstitial activator A, transforming growth factor-β1 and monocyte chemokine protein-1. It can also participate in the reconstruction of the glomerular extracellular matrix by affecting the expression of protein kinase ERK1/2 protein, which serves a protective effect on diabetic kidneys. Tanshinone can inhibit oxidative stress mediated glucose-induced kidney injury, inhibit the expression of protein tyrosine phosphatase 1B (PTP1B) activity, and improve the secretion function of beta cells in type 2 diabetes mellitus. Interstitial fibrosis in diabetic nephropathy can be alleviated by blocking TGF-β/Smad, NF-κB and Wnt/β-catenin signaling pathway. It has been suggested that salvianolic acid and salvianone are excellent candidates for prevention and treatment of diabetic nephropathy. We provide here the scientific basis for in-depth research and development of salvianolic acid and salvianone into drugs.

     

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