|
|
|
| Mechanism of Sanqi Oral Liquid in the treatment of diabetic nephropathy based on network pharmacology |
| LIN Jiarong1 ZHANG Lei2 GUI Dingkun3 ZENG Guixing1 WU Yuchi2 ZOU Chuan2 LIN Qizhan2 |
1.The Second Clinical Medical College, Guangzhou University of Chinese Medicine, Guangdong Province, Guangzhou 510405, China;
2.Department of Nephrology, the Second Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangdong Province, Guangzhou 510120, China; 3.Department of Nephrology, the Sixth People′s Hospital Affiliated to Shanghai Jiaotong University, Shanghai 200233, China |
|
|
|
Abstract Objective To explore the mechanism of Sanqi Oral Liquid in the treatment of diabetic nephropathy. Methods According to the ADME characteristics of the drug, TCMSP platform was used to screen the active ingredients and targets of Sanqi Oral Liquid, which was developed with the compound of Sanqi and Huangqi, and the component target network was constructed. Retrieval of diabetic nephropathy related targets based on GeneCards database, DisGeNET database and OMIM database. The target of active drugs, active ingredients and genes was constructed by using the software of Cytoscape, and the target information was analyzed by using the database of DAVID and the biological process and pathway enrichment were analyzed. Results There were 27 active components were screened, involving 191 targets, and 118 potential targets related to disease targets. The therapeutic effect of diabetic nephropathy was mainly achieved by regulating PPARG, IL-6 and age-range signaling pathway, fluid shear stress and atherosclerosis, IL-17 signaling pathway, HIF-1 signaling pathway, etc. Conclusion Sanqi Oral Liquid can treat diabetic nephropathy through multi-target and multi-channel, which provides theoretical basis and scientific basis for explaining its therapeutic mechanism.
|
|
|
|
|
|
[1] Zhang L，Wang F，Wang L，et al. Prevalence of chronic kidney disease in China：a cross-sectional survey [J]. Lancet，2012，379（9818）：815-822.
[2] Liu ZH. Nephrology in china [J]. Nat Rev Nephrol，2013， 9（9）：523-528.
[3] KDOQI Clinical Practice Guidelines and Clinical Practice Recommendations for Diabetes and Chronic Kidney Disease [J]. Am J Kidney Dis，2007，49（2 Suppl 2）：S12-S154.
[4] 王晓光，王亚丽，张佩清.张琪教授辨治糖尿病肾病经验介绍[J].新中医，2005（3）：20-21.
[5] 张再康，杨霓芝，苏敬文，等.通脉口服液防治Ⅱ期糖尿病肾病的药效学研究[J].中国中医药信息杂志，2009，16（3）：32-34.
[6] Ru J，Li P，Wang J，et al. TCMSP：a database of systems pharmacology for drug discovery from herbal medicines [J]. J Cheminform，2014，6：13.
[7] 张再康，杨霓芝，王立新，等.杨霓芝应用益气活血法治疗糖尿病肾病的学术思想探讨[J].中国中医基础医学杂志，2009，15（8）：603-604.
[8] 范萍，袁海英，祝勇军，等.益气活血法治疗气虚血瘀型糖尿病肾病临床研究[J].中国中医急症，2009，18（3）：367-369.
[9] 范萍，郝莉，郑发春，等.通脉口服液干预实验性糖尿病肾病模型大鼠的实验研究[J].中国中医急症，2009，18（1）：93-95.
[10] 范萍，杨霓芝.通脉口服液对实验性DN模型大鼠肾组织Col-Ⅳ及MMP-9/TIMP-1的影响[J].中国中西医结合肾病杂志，2010，11（1）：7-9.
[11] 范萍，杨霓芝.通脉口服液对实验性糖尿病肾病模型大鼠肾脏病理及转化生长因子β1的影响[J].广州中医药大学学报，2008（6）：514-518.
[12] Lu Q，Ji XJ，Zhou YX，et al. Quercetin inhibits the mTORC1/p70S6K signaling-mediated renal tubular epithelial-mesenchymal transition and renal fibrosis in diabetic nephropathy [J]. Pharmacol Res，2015，99：237-247.
[13] Tong F，Liu S，Yan B，et al. Quercetin nanoparticle complex attenuated diabetic nephropathy via regulating the expression level of ICAM-1 on endothelium [J]. Int J Nanomedicine，2017，12：7799-7813.
[14] Sharma D，Gondaliya P，Tiwari V，et al. Kaempferol attenuates diabetic nephropathy by inhibiting RhoA/Rho-kinase mediated inflammatory signalling [J]. Biomed Pharmacother，2019，109：1610-1619.
[15] Oza MJ，Kulkarni YA. Formononetin attenuates kidney damage in type 2 diabetic rats [J]. Life Sci，2019，219：109-121.
[16] Qiu S，Sun G，Zhang Y，et al. Involvement of the NF-kappaB signaling pathway in the renoprotective effects of isorhamnetin in a type 2 diabetic rat model [J]. Biomed Rep，2016，4（5）：628-634.
[17] Liu L，Zheng T，Wang F，et al. Pro12Ala polymorphism in the PPARG gene contributes to the development of diabetic nephropathy in Chinese type 2 diabetic patients [J]. Diabetes Care，2010，33（1）：144-149.
[18] Chang WT，Huang MC，Chung HF，et al. Interleukin-6 gene polymorphisms correlate with the progression of nephropathy in Chinese patients with type 2 diabetes：a prospective cohort study [J]. Diabetes Res Clin Pract，2016，120：15-23.
[19] Ururahy MA，de Souza KS，Oliveira YM，et al. Association of polymorphisms in IL-6 gene promoter region with type 1 diabetes and increased albumin-to-creatinine ratio [J]. Diabetes Metab Res Rev，2015，31（5）：500-506.
[20] Ramasamy R，Yan SF，Schmidt AM. Receptor for AGE （RAGE）：signaling mechanisms in the pathogenesis of diabetes and its complications [J]. Ann N Y Acad Sci，2011， 1243：88-102.
[21] Yamagishi S. Role of advanced glycation end products （AGEs） and receptor for AGEs （RAGE） in vascular damage in diabetes [J]. Exp Gerontol，2011，46（4）：217-224.
[22] Thomas MC，Woodward M，Neal B，et al. Relationship between levels of advanced glycation end products and their soluble receptor and adverse outcomes in adults with type 2 diabetes [J]. Diabetes Care，2015，38（10）：1891-1897.
[23] Assmann TS，Recamonde-Mendoza M，Costa AR，et al. Circulating miRNAs in diabetic kidney disease：case-control study and in silico analyses [J]. Acta Diabetol，2019，56（1）：55-65.
[24] Kuo HL，Huang CC，Lin TY，et al. IL-17 and CD40 ligand synergistically stimulate the chronicity of diabetic nephropathy [J]. Nephrol Dial Transplant，2018，33（2）：248-256.
[25] Ma J，Li YJ，Chen X，et al. Interleukin 17A promotes diabetic kidney injury [J]. Sci Rep，2019，9（1）：2264.
[26] Cortvrindt C，Speeckaert R，Moerman A，et al. The role of interleukin-17A in the pathogenesis of kidney diseases [J]. Pathology，2017，49（3）：247-258.
[27] Mohamed R，Jayakumar C，Chen F，et al. Low-dose IL-17 therapy prevents and reverses diabetic nephropathy，metabolic syndrome，and associated organ fibrosis [J]. J Am Soc Nephrol，2016，27（3）：745-765.
[28] Galvan DL，Danesh FR. Paradoxical role of IL-17 in progression of diabetic nephropathy [J]. J Am Soc Nephrol，2016，27（3）：657-658.
[29] Nayak BK，Shanmugasundaram K，Friedrichs WE，et al. HIF-1 mediates renal fibrosis in OVE26 type 1 diabetic mice [J]. Diabetes，2016，65（5）：1387-1397.
[30] Persson P，Palm F. Hypoxia-inducible factor activation in diabetic kidney disease [J]. Curr Opin Nephrol Hypertens，2017，26（5）：345-350. |
|
|
|
