Ursolic acid alleviates isoproterenol-induced kidney injury in mice by suppressing inflammation, apoptosis, and oxidative stress via the PI3K/Akt signaling

Objective: To investigate the protective effect of ursolic acid (UA) on isoproterenol (ISO)-induced kidney injury in mice. Methods: Four groups of mice were used: Group I (Control) received phosphate-buffered saline i.p. for four weeks; Group II (ISO alone) was administered ISO (10 mg/kg i.p. ) daily for four weeks to induce kidney injury; Group III (ISO+UA) was pretreated with UA (40 mg/kg i.p. ) once daily, followed by ISO (10 mg/kg i.p. ) once daily for four weeks; Group IV (UA alone) received UA (40 mg/kg i.p. ) daily for four weeks. Markers of oxidative stress, inflammation, and apoptosis were analyzed, and the protein expression of p-PI3K and p-Akt was determined. Results: UA treatment significantly alleviated ISO-induced kidney injury, evidenced by lowered levels of malondialdehyde, IL-6, TNF-α and IL-Iβ, downregulated expression of cleaved caspase-3 and PARP, and upregulated expression of Bcl-2 and Bcl-xL. It also activated the PI3K/Akt pathway. Conclusions: UA demonstrates renoprotective effects against ISO-induced kidney injury by reducing oxidative stress, inflammation, and apoptosis, likely through PI3K/Akt pathway activation. These findings suggest that UA may serve as a potential therapeutic agent for renal diseases linked to inflammation and oxidative stress, meriting further exploration for clinical applications.