Exploring the Potential Mechanism of Tang-Shen-Ning Decoction against Diabetic Nephropathy Based on the Combination of Network Pharmacology and Experimental Validation | Zendy

Jiajun Liang | Zendy; Jiaxin He | Zendy; Yanbin Gao | Zendy; Zhiyao Zhu | Zendy

Open Access

Exploring the Potential Mechanism of Tang-Shen-Ning Decoction against Diabetic Nephropathy Based on the Combination of Network Pharmacology and Experimental Validation

Author(s) -

Jiajun Liang,

Jiaxin He,

Yanbin Gao,

Zhiyao Zhu

Publication year - 2021

Publication title -

evidence-based complementary and alternative medicine

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 0.552

H-Index - 90

eISSN - 1741-4288

pISSN - 1741-427X

DOI - 10.1155/2021/1025053

Subject(s) - ctgf , diabetic nephropathy , renal function , fibrosis , mechanism (biology) , pharmacology , kegg , medicine , kidney , chemistry , gene , growth factor , biochemistry , receptor , gene ontology , philosophy , epistemology , gene expression

Background Diabetic nephropathy (DN) has become one of the leading causes of the end-stage renal disease (ESRD). Tang-Shen-Ning (TSN) decoction, an effective Traditional Chinese formula for DN, can improve the renal function and inhibit renal fibrosis in DN. However, its potential mechanism is still unexplored.Methods A network pharmacology approach was employed in this study, including screening for differential expressed genes of DN (DN-DEGs), protein-protein interaction (PPI) network analysis, and GO and KEGG enrichment analysis. Besides, a rat model was established to verify the potential effect of TSN in DN.Results Twenty-three TSN-related DN-DEGs targets were identified. These genes were associated with decreased glomerular filtration rate (GFR) DN. The enrichment analysis suggested that the inhibition of renal fibrosis and inflammation through growth factors and chemokines is the potential mechanism through which TSN improves DN. TSN reduced renal fibrosis and improved pathological damage in the kidney in vivo through the regulation of GJA1, CTGF, MMP7, and CCL5, which are genes associated with ECM deposition.Conclusion This study revealed that TSN improves DN through a multicomponent, multitarget, and multipathway synergy. We provide a scientific basis for potential targets for TSN use to treat DN, yet further experimental validation is needed to investigate these targets and mechanisms.

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