Syringaldehyde attenuates deltamethrin-induced hepatic tissue injury by modulating oxidative stress, inflammation,...

Exposure to pesticides poses a substantial global public health challenge. Among these agents, deltamethrin (DEL), a commonly applied synthetic pyrethroid in agricultural practices, has attracted particular concern due to its bioaccumulative potential and its capacity to induce cellular injury via oxidative stress mechanisms, with the liver being especially vulnerable. Syringaldehyde (SYR) is a naturally derived polyphenolic compound within the flavonoid class and has been reported to exhibit therapeutic properties in various pathological conditions. The current investigation was designed to evaluate the hepatoprotective efficacy of SYR and to clarify the underlying mechanisms involved in DEL-induced hepatic damage. Experimental hepatotoxicity was established in mice by intragastric administration of DEL (15 mg/kg). SYR was administered orally at doses of 25 and 50 mg/kg, while silymarin (50 mg/kg) served as a reference hepatoprotective agent. DEL exposure produced marked elevations in serum liver enzymes (AST, ALT, and ALP), lipid peroxidation indices (MDA), nitric oxide levels, pro-inflammatory mediators (NFκB, iNOS, Cox-2, TNF-α, IL-1β, and IL-6), and pro-apoptotic proteins (Bax and Cas-3). Concurrently, significant reductions were observed in GSH, SOD, and CAT, PGE2, and the expression of cytoprotective and anti-apoptotic markers, including Nrf2, HO-1, and Bcl-2. In comparison with the DEL-treated group, SYR supplementation markedly mitigated hepatic enzyme leakage, inflammatory and oxidative stress markers, and apoptotic protein expression, while restoring antioxidant capacity, PGE2 levels, and the expression of Nrf2, HO-1, and Bcl-2. Collectively, these findings provide strong evidence that SYR confers protection against DEL-induced liver injury in mice, primarily through modulation of the Nrf2/HO-1 signaling pathway.