ArticleMolecular and cellular biochemistry2026
TangShenKang decoction plays an anti-inflammatory and anti-fibrotic role in diabetic nephropathy by activating AT2R/ATIP1/SHP1 axis and antagonizing angiotensin II.
Article in Molecular and cellular biochemistry, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Diabetic nephropathy (DN) is the most prevalent microvascular complication of diabetes, where a hyperglycemic environment can induce chronic damage to renal vessels and parenchyma, severely endangering patients' health. TangShenKang decoction (TSK) is a traditional Chinese medicine formula developed based on the clinical and pathological characteristics of DN. In this study, through transcriptomic data analysis of a rat DN model and a TSK intervention group, the key regulatory gene AT2R was identified. Molecular mechanisms underlying TSK's effects on inflammation and fibrosis in DN were investigated using Western blot, quantitative polymerase chain reaction (qPCR), and immunofluorescence staining experiments, with further in vivo validation of TSK's therapeutic effects on DN. The results showed that TSK can activate AT2R in the DN model and promote SHP1 phosphorylation, thereby inhibiting the phosphorylation of IκBα, an important protein in the NFκB signaling pathway, reducing the secretion of inflammatory cytokines such as TNF-α, IL-1β, and IL-6, and suppressing the progression of inflammation. Meanwhile, after activating AT2R, TSK can effectively inhibit the epithelial-mesenchymal transition (EMT) process in DN, downregulate the expression of p-Smad2/3 in the TGF-β signaling axis, and decrease the expression levels of fibrosis phenotype molecules such as connective tissue growth factor (CTGF), platelet-derived growth factor (PDGF), and fibronectin 1 (FN1), thereby alleviating renal fibrosis in DN. In conclusion, the therapeutic effect of TSK on DN may be mediated through the activation of the AT2R/ATIP1/SHP1 axis, which subsequently inhibits inflammation- and fibrosis-related signaling pathways.
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