Effects of Borage Oil on Oxidative Damage, Inflammatory Response (IL-6, IL-1β, and TNF- α), and Signaling Pathways (Bax/Bcl-2 and Caspase-3) in Lead Acetate–Induced Nephrotoxicity

Objective: In this study, the potential protective effects of borage oil (BO), a plant-derived oil of medical and nutritional importance, against lead acetate–induced nephrotoxicity were investigated. Methods: In the experimental model, biochemical alterations related to oxidative stress and the antioxidant defence system in rat kidney tissue were evaluated. A total of 30 Sprague Dawley rats were randomly assigned to five experimental groups. Nephrotoxicity was induced by intraperitoneal administration of lead acetate at a dose of 20 mg/kg for 7 days. Borage seed oil was administered orally at doses of 50 and 100 mg/kg for 14 days. Malondialdehyde (MDA) levels, a marker of lipid peroxidation in kidney tissue, were determined using ELISA, while the expression levels of SOD, CAT, and GPx, as well as the gene expression levels of Bax, Bcl-2, and caspase-3, were analysed by RT-PCR. In addition, protein expression levels of inflammatory markers associated with the inflammatory response, including IL-6, IL-1β, and TNF-α, were evaluated by Western blot analysis. Results: The results demonstrated that lead acetate increased oxidative stress in kidney tissue, whereas borage oil enhanced antioxidant defense mechanisms and reduced lipid peroxidation. Lead exposure increased the expression of apoptotic markers (Bax and caspase-3) and decreased Bcl-2 expression in renal tissue, while borage oil—particularly at the 100 mg/kg dose—significantly reversed these alterations and markedly suppressed apoptosis. Furthermore, lead exposure significantly increased the expression of pro-inflammatory markers in kidney tissue, whereas borage oil attenuated this increase, particularly for TNF-α and IL-1β (and IL-6 at the higher dose), thereby modulating the lead-induced inflammatory response. Conclusion: Borage oil exhibited a protective effect against lead acetate–induced renal injury and may alleviate nephrotoxicity.