Salt-stir fried Eucommiae Cortex (SEC) more potently inhibits renal fibrosis and EMT than raw form in rat model

Renal fibrosis is a progressive and irreversible condition leading to end-stage renal disease, characterized by excessive accumulation of extracellular matrix proteins. A key driver of this progression is epithelial-mesenchymal transition (EMT), where renal tubular epithelial cells lose their epithelial characteristics and acquire a mesenchymal phenotype, contributing to scar tissue formation. Current treatments often fall short in fully halting or reversing fibrosis. Eucommiae Cortex (EC), a traditional Chinese medicine, has shown renoprotective effects, but its processed form, salt-stir fried Eucommiae Cortex (SEC), is hypothesized to offer enhanced therapeutic efficacy, addressing a critical gap in optimizing natural product interventions for renal fibrosis.

Researchers compared the effects of Eucommiae Cortex (EC) and salt-stir fried Eucommiae Cortex (SEC) on adenine-induced renal fibrosis in rats. Rats were divided into blank control, model, positive drug, and low, medium, and high-dose EC and SEC groups. Fibrosis markers (α-SMA, collagen Ⅰ, fibronectin, vimentin) were detected in renal tissue using Western blot and immunofluorescence. Transcriptional expression of EMT factors (Snai1, Twist1, ZEB1) and inflammatory factors (TNF-α, IL-1β, IL-6) was measured by Real-time fluorescent quantitative reverse transcription PCR. In vitro, TGF-β-stimulated NRK-52E renal tubular epithelial cells were used to evaluate EC and SEC's inhibitory effects on fibrosis markers and EMT, with network pharmacology and Western blot exploring mechanisms.

Both Eucommiae Cortex (EC) and salt-stir fried Eucommiae Cortex (SEC) significantly ameliorated adenine-induced renal fibrosis in rats and TGF-β-stimulated NRK-52E cells. They notably reduced protein expression of fibrosis markers including fibronectin, collagen Ⅰ, vimentin, and α-SMA. Furthermore, both forms inhibited the transcriptional expression of key EMT transcription factors such as Snai1, Twist1, and ZEB1. Inflammatory factors, specifically TNF-α, IL-1β, and IL-6, also saw reduced transcriptional expression. The study consistently found that the inhibitory effects of SEC were stronger than those of EC across all measured parameters. This enhanced efficacy of SEC was further supported by network pharmacology analysis, suggesting a more potent modulation of underlying molecular mechanisms.

The inhibitory effects of salt-stir fried Eucommiae Cortex (SEC) were consistently stronger than those of raw Eucommiae Cortex (EC) in reducing fibrosis markers, EMT transcription factors, and inflammatory cytokines.