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Natural products in traditional Chinese medicine: molecular mechanisms and therapeutic targets of renal fibrosis and state-of-the-art drug delivery systems - 05/01/24

Doi : 10.1016/j.biopha.2023.116039 
Li Song a, 1, Wei Zhang a, 1, Shi-yun Tang b, 1, Si-min Luo c, Pei-yu Xiong a, Jun-yu Liu a, Heng-chang Hu a, Ying-qi Chen c, Bo Jia a, Qian-hua Yan d, , Song-qi Tang c, , Wei Huang a,
a College of Basic Medicine, Chengdu University of Traditional Chinese Medicine, Chengdu 611137, China 
b Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 610032, China 
c College of Traditional Chinese Medicine, Hainan Medical University, Haikou 571199, China 
d Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing 210000, China 

Corresponding authors.

Abstract

Renal fibrosis (RF) is the end stage of several chronic kidney diseases. Its series of changes include excessive accumulation of extracellular matrix, epithelial-mesenchymal transition (EMT) of renal tubular cells, fibroblast activation, immune cell infiltration, and renal cell apoptosis. RF can eventually lead to renal dysfunction or even renal failure. A large body of evidence suggests that natural products in traditional Chinese medicine (TCM) have great potential for treating RF. In this article, we first describe the recent advances in RF treatment by several natural products and clarify their mechanisms of action. They can ameliorate the RF disease phenotype, which includes apoptosis, endoplasmic reticulum stress, and EMT, by affecting relevant signaling pathways and molecular targets, thereby delaying or reversing fibrosis. We also present the roles of nanodrug delivery systems, which have been explored to address the drawback of low oral bioavailability of natural products. This may provide new ideas for using natural products for RF treatment. Finally, we provide new insights into the clinical prospects of herbal natural products.

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Graphical Abstract




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Fig. 1. Pectolinarigenin; PUE: Puerarin; QUE: Quercetin; ISL: Isoliquiritigenin; CA: Calycosin; DHM: Dihydromyricetin; API: Apigenin; DHQ: Dihydroquercetin; TS IIA: Tanshinone IIA; RH: Rhein; EMD: Emodin; CP: Chrysophanol; CUR: Curcumin; RSV: Resveratrol; SAB: Salvianolic acid B; EGCG: Epigallocatechin-3-Gallate; SAL: Salidroside; AS IV: Astragaloside IV; Rg1: Ginsenoside Rg1; BBR: Berberine; OM: Oxymatrine; SIN: Sinomenine; DHA: Dihydroartemisinin; ART: Artemisinin; GAA: Ganoderic acid A; TP: Triptolide; PAA: Poricoic acid A.


Fig. 1. Pectolinarigenin; PUE: Puerarin; QUE: Quercetin; ISL: Isoliquiritigenin; CA: Calycosin; DHM: Dihydromyricetin; API: Apigenin; DHQ: Dihydroquercetin; TS IIA: Tanshinone IIA; RH: Rhein; EMD: Emodin; CP: Chrysophanol; CUR: Curcumin; RSV: Resveratrol; SAB: Salvianolic acid B; EGCG: Epigallocatechin-3-Gallate; SAL: Salidroside; AS IV: Astragaloside IV; Rg1: Ginsenoside Rg1; BBR: Berberine; OM: Oxymatrine; SIN: Sinomenine; DHA: Dihydroartemisinin; ART: Artemisinin; GAA: Ganoderic acid A; TP: Triptolide; PAA: Poricoic acid A.ga1

Le texte complet de cet article est disponible en PDF.

Highlights

There is abundant evidence that natural products of Chinese medicines have reversal or delaying effects on renal fibrosis.
Natural products can play therapeutic roles in treating various causes of renal fibrosis through different signaling pathways.
Nano-delivery systems can help address the low bioavailability of natural products, making the treatment of renal fibrosis with Chinese medicine more promising.

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Chemical compounds studied in this article : Pectolinarigenin (Pubmed CID: 5320438), Puerarin (Pubmed CID: 5281807), Quercetin (Pubmed CID: 5280343), Isoliquiritigenin (Pubmed CID: 638278), Calycosin (Pubmed CID: 5280448);Dihydromyricetin (Pubmed CID: 161557), Apigenin (Pubmed CID: 5280443), Dihydroquercetin (Pubmed CID: 439533), Tanshinone IIA (Pubmed CID: 164676), Rhein (Pubmed CID: 10168), Emodin (Pubmed CID: 3220), Chrysophanol (Pubmed CID: 10208), Curcumin (Pubmed CID: 969516), Resveratrol (Pubmed CID: 445154), Salvianolic acid B (Pubmed CID: 6541084), Epigallocatechin-3-Gallate (Pubmed CID: 65064), Salidroside (Pubmed CID: 159278), Astragaloside IV (Pubmed CID: 13943297), Ginsenoside Rg1 (Pubmed CID: 441923), Berberine (Pubmed CID: 2353), Oxymatrine (Pubmed CID: 114850)

Abbreviations : RF, CDK, ECM, TCM, ERS, JAK, STAT, MAPK, PI3K, ROS, EMT, FSP-1, HSP 47, Col1α1, PDGFRβ, PDGFRα, MEG3, COLEC11, CXCL12, RGS5, TGF-β, HER2, CTGF, TIMP, LCN2, INHBB, α-SMA, FN, TNC, RAS, SGLT2, GLP-1, ET-1, NRF2, NF-κB, TLR4, MyD88, IRF5, SIRT1, PINK1, Syk, IL-33, ST2, TNFR1, NOX2, HO-1, URAT1, GLUT9, TRPV4, TNF-α, AMPK, ERK1/2, NLRP3, MCP-1, PERK, elF2a, ATF4, SHH, Gli1, PPARα, CPTIa, ACOX1, Bcl-2, Bax, STRT1, CREB, BMP, mTOR, HGF, Smurf2, HMGA2, EZH2, NKD2, Cav-1, Keap 1, APPL1, LC3 II, RGMb, SphK1, S1P, foxo3a, HPSE, PDGF-C, GSK-3β, ACTN4, VEGF, DNMT, PGC1-α, Cx43, mTORC1, TSP-1, TRPC6, NFAT2, MMP2, RhoA, ROCK, P2×7R, MDM2, DUSP6, SnoN, Id2, LN, IL-6, ICAM-1, SOCS1, DNMT1, TRX, TRXR, PTEN, TPH-1, UUO, HEK293, NRK-49 F, cAMP, HK-2, RTEC, DN, COL III, HFD, STZ, BMSC, PTEC, NADPH, DKD, VDR, HG, NRK-52E, ConA, C3aR, C5aR, suPAR, h3k27me3, FA, RSK2, T2DM, MN, TGFR, AKI, JNK, SAPK, cPLA2, EGFR, CTMP, NDSS, SLN, CS

Keywords : Renal fibrosis, Natural products, Flavonoids, Phenols, NDSS


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