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The Role of Brucine A in Renal Fibrosis

GSE339176 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/07/25 Platform GPL24247
Summary
Renal fibrosis is the common pathological basis for the progression of various chronic kidney diseases to end-stage renal disease, which is mainly manifested as renal tissue inflammatory infiltration, oxidative stress imbalance, renal tubular epithelial cell transdifferentiation and excessive extracellular matrix deposition. Currently, there are no effective targeted reversal methods in clinical practice. Brucine A (BA), a natural triterpenoid active ingredient, possesses significant anti-inflammatory, antioxidant and anti-fibrotic pharmacological activities. It can inhibit renal inflammatory responses and oxidative stress damage, reduce the expression of fibrosis-related proteins and matrix accumulation by regulating key signaling pathways such as TGF-beta1 and NF-kB, thereby effectively delaying the progression of renal fibrosis. This study aims to systematically clarify the intervention effect of BA on renal fibrosis and reveal its potential molecular mechanism, so as to provide experimental evidence and theoretical basis for the prevention and treatment of chronic kidney diseases as well as the clinical transformation and application of BA.
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Direct links to NCBI, no account and no request form: the whole study as GSE339176_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 6 samples. Raw sequencing reads are also available from ENA.

Also filed as BioProject PRJNA1497588 and SRA study SRP719410. Searching any of these in the dataset finder brings you back here.

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