Metabolic dysfunction-associated steatotic liver disease (MASLD) poses a global health threat, necessitating natural therapeutics. Rosa roxburghii Tratt (RRT), a medicinal and edible resource, shows anti-MASLD potential but lacks defined bioactive components and mechanisms. Using UHPLC-HRMS analysis and network pharmacology, we identified ellagic acid (EA) as RRT’s primary bioactive component against MASLD. In high-fat diet (HFD)-fed mice and oleic acid (OA)-induced hepatocytes, EA alleviated hepatic steatosis, reduced serum and liver triglycerides (TG) and total cholesterol (TC), and lipid droplet-associated marker Plin2 expression. Mechanistically, EA inhibited PPARγ transcription and translation, and concurrently downregulated the mRNA expression of lipid metabolism–related genes associated with the PPARγ signaling pathway (Cebpa, Acc1, Fasn, Cd36, Hmgcr, Srebf2) in MASLD mice. Similar regulatory effects were also observed in two hepatic cell-based MASLD models (Acc1, Hmgcr and Srebf2). Pharmacological studies with PPARγ agonist (pioglitazone) and antagonist (GW9662) confirmed EA counteracts lipid dysregulation via PPARγ-dependency. This work establishes EA as a novel PPARγ-targeting phytochemical restoring hepatic lipid homeostasis, providing a molecular foundation for plant-derived MASLD interventions and highlighting RRT’s translational promise.

A high-fat diet (HFD) has been implicated in the development of prostatic fibrosis, which, either independently or in combination with benign prostatic hyperplasia (BPH), can result in lower urinary tract symptoms (LUTS) in elderly men. Rosa roxburghii Tratt (RRT), a food with both edible and medicinal properties, is rich in a diverse range of bioactive compounds, including terpenoids, organic acids, polyphenols, coumarins, glycosides, amino acids, flavonoids, and phthalides. In this study, we employed an HFD-induced prostatic fibrosis mouse model to investigate the anti-fibrotic effects of RRT extracts and the underlying mechanisms. Treatment with RRT extracts mitigated the progression of prostatic fibrosis by addressing lipid metabolic dysregulation, inflammation, oxidative stress, and imbalances in sex hormone levels. Furthermore, RRT extracts reduced the incidence of bladder urine retention in HFD-fed mice and inhibited the TGF-β/Smad signaling pathway, a key mediator of fibrosis. Collectively, these findings suggest that RRT extracts may ameliorate HFD-induced prostatic fibrosis through a multi-target, multi-component approach. This study provides valuable experimental insights into the pathogenesis of HFD-induced prostatic fibrosis and supports the potential therapeutic application of RRT in health, food, and medicinal contexts.