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Advances in Oxidative Stress in Pathogenesis of Diabetic Kidney Disease and Efficacy of TCM Intervention

Overview
Journal Ren Fail
Publisher Informa Healthcare
Date 2023 Feb 10
PMID 36762989
Authors
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Abstract

Diabetic kidney disease (DKD) is a common complication of diabetes and has become the leading cause of end-stage kidney disease. The pathogenesis of DKD is complicated, and oxidative stress is considered as a core of DKD onset. High glucose can lead to increased production of reactive oxygen species (ROS) the polyol, PKC, AGE/RAGE and hexosamine pathways, resulting in enhanced oxidative stress response. In this way, pathways such as PI3K/Akt, TGF-β1/p38-MAPK and NF-κB are activated, inducing endothelial cell apoptosis, inflammation, autophagy and fibrosis that cause histologic and functional abnormalities of the kidney and finally result in kidney injury. Presently, the treatment for DKD remains an unresolved issue. Traditional Chinese medicine (TCM) has unique advantages for DKD prevention and treatment attributed to its multi-target, multi-component, and multi-pathway characteristics. Numerous studies have proved that Chinese herbs (e.g., Golden Thread, Kudzuvine Root, Tripterygium glycosides, and Ginseng) and patent medicines (e.g., Shenshuaining Tablet, Compound Rhizoma Coptidis Capsule, and Zishen Tongluo Granule) are effective for DKD treatment. The present review described the role of oxidative stress in DKD pathogenesis and the effect of TCM intervention for DKD prevention and treatment, in an attempt to provide evidence for clinical practice.

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References
1.
Mao C, Gu Z . Puerarin reduces increased c-fos, c-jun, and type IV collagen expression caused by high glucose in glomerular mesangial cells. Acta Pharmacol Sin. 2005; 26(8):982-6. DOI: 10.1111/j.1745-7254.2005.00133.x. View

2.
Singh L, Cheng D, Kowluru R, Levi E, Jiang Y . Hexosamine induction of oxidative stress, hypertrophy and laminin expression in renal mesangial cells: effect of the anti-oxidant alpha-lipoic acid. Cell Biochem Funct. 2006; 25(5):537-50. DOI: 10.1002/cbf.1358. View

3.
Su J, Gao C, Xie L, Fan Y, Shen Y, Huang Q . Astragaloside II Ameliorated Podocyte Injury and Mitochondrial Dysfunction in Streptozotocin-Induced Diabetic Rats. Front Pharmacol. 2021; 12:638422. PMC: 8008105. DOI: 10.3389/fphar.2021.638422. View

4.
Yu J, Wu H, Liu Z, Zhu Q, Shan C, Zhang K . Advanced glycation end products induce the apoptosis of and inflammation in mouse podocytes through CXCL9-mediated JAK2/STAT3 pathway activation. Int J Mol Med. 2017; 40(4):1185-1193. PMC: 5593472. DOI: 10.3892/ijmm.2017.3098. View

5.
Feng H, Zhu X, Tang Y, Fu S, Kong B, Liu X . Astragaloside IV ameliorates diabetic nephropathy in mice by inhibiting NLRP3 inflammasome‑mediated inflammation. Int J Mol Med. 2021; 48(2). PMC: 8262660. DOI: 10.3892/ijmm.2021.4996. View