Therapeutic potential of Desmodium styracifolium polysaccharide in attenuating nano-calcium oxalate induced renal injury and fibrosis.

Calcium salt deposition in the kidney induces epithelial-to-mesenchymal transition (EMT) in renal tubular epithelial cells, which is the pathological basis for the progression to renal fibrosis in patients with renal stones; however, effective drugs to prevent and treat this disease have not been adequately investigated. In this study, we conducted a comprehensive analysis of fibrosis-related core genes by utilizing bioinformatics on RNA-seq data, along with web database information. Additionally, we designed both in vivo and in vitro experiments to elucidate the mechanisms and signaling pathways through which Desmodium styracifolium polysaccharides (Ds) mitigate renal fibrosis induced by nephrolithiasis. Renal fibrosis is present in both patients afflicted with calcium oxalate (CaOx) stones and in model rats. RNA-seq analysis and network database examination identified TGF-β as a fibrosis-related core gene. Moreover, Ds were found to accumulate in the kidneys of these model rats, effectively reducing crystalline deposits, mitigating renal injury, and alleviating renal fibrosis. Ds effectively attenuated nano-CaOx-induced HK-2 damage and delayed the EMT process by interfering with TGF-β expression and secretion and inhibiting the activation of the TGF-β/Smad pathway in vitro. Ds may emerge as a potential therapeutic option for the clinical treatment of crystalline renal fibrosis.