@article{article_1692921, title={Investigation of the Effects of Syringic Acid on Oxidative Stress, Cytokines, Apoptosis and Inflammation Against Cadmium-Induced Hepatotoxicity in Rats}, journal={Erciyes Üniversitesi Veteriner Fakültesi Dergisi}, volume={22}, pages={177–188}, year={2025}, DOI={10.32707/ercivet.1692921}, url={https://izlik.org/JA54YM73EB}, author={Karaarslan, Tuba and Aktas Senocak, Esra and Alat, Ömercan and Halıcı, Mesut Bünyami}, keywords={Antioksidan, Kadmiyum, Sitokin, İnflamasyon, Oksidatif stres.}, abstract={Cadmium (Cd) is a toxic heavy metal and a significant environmental contaminant known to cause hepatotoxicity through mechanisms involving oxidative stress, inflammation, and apoptosis. Syringic acid (Sa), a naturally occurring phenolic compound, exhibits potent antioxidant and anti-inflammatory activities. This study aimed to evaluate the protective effects of SA against Cd-induced liver injury in rats. Fifty adult male Sprague-Dawley rats were randomly allocated into five groups (n= 10 per group): Control, Sa 100, Cd, Sa 50+Cd and Sa 100+Cd. Cadmium and/or SA were administered orally for 7 consecutive days. Biochemical markers of oxidative stress (SOD, GSH, CAT, and MDA), pro-inflammatory cytokines (TNF-α, IL-1β, IL-6), and molecular indicators of inflammation (TLR-4, NF-κB) and apoptosis (Bax, Bcl-2, Caspase-3) were measured in liver tissue homogenates. Cadmium exposure significantly decreased the hepatic antioxidant enzyme activities (SOD, GSH, and CAT) and increased MDA and TLR-4 levels, indicating enhanced oxidative damage and inflammatory activation. Additionally, NF-κB, TNF-α, IL-1β, and IL-6 levels were markedly elevated following Cd administration. Apoptotic changes were evident by increased Bax and Caspase-3 expression and decreased Bcl-2 levels. Syringic acid co-administration dose-dependently ameliorated these pathological alterations, restoring oxidative balance, suppressing inflammation, and modulating apoptotic signaling. Syringic acid effectively attenuates cadmium-induced liver toxicity in rats by mitigating oxidative stress, suppressing pro-inflammatory responses, and regulating apoptosis-related pathways. These findings suggest that SA may serve as a promising hepatoprotective agent in conditions of heavy metal-induced hepatic injury.}, number={3}