The current study investigated the anti-inflammatory and antioxidant activities of taurine (Tau), a semi-essential amino acid, against tartrazine (Tz)-induced hepatic injury, with particular emphasis on the SIRT-1/HMGB-1 signaling pathway. Twenty-eight male albino rats were randomly divided into four groups (n = 7/group): Control, Tau (100 mg/kg/day), Tz (7.5 mg/kg/day), and Tz+Tau, all administered orally by gavage for 30 days. Tz exposure induced significant hepatotoxicity, evidenced by body weight loss, increased relative liver weight, and marked elevation of serum liver enzymes. Tz also provoked severe oxidative stress, as indicated by a 344.76% increase in hepatic MDA, with significant depletion of antioxidant defenses: SOD (82.31%), CAT (60.53%), GPx (44.45%), and GSH (92.18%) relative to control. In addition, Tz markedly suppressed hepatic SIRT-1 mRNA expression (75.51%), accompanied by architectural disruption, inflammatory cell infiltration, necrosis, increased collagen deposition, and upregulation of HMGB-1, TGF-β1, TNF-α, and α-SMA. Conversely, taurine coadministration significantly ameliorated these alterations, reducing elevated liver enzymes by 22.29% (ALT), 49.22% (AST), and 35.21% (GGT), lowering MDA by 52.17%, and restoring antioxidant status with increases of 213.27% (SOD), 101.92% (CAT), 44.55% (GPx), and 565.91% (GSH) compared with the Tz group. Taurine also partially restored SIRT-1 mRNA expression by 220.8% relative to Tz and significantly attenuated fibrosis- and inflammation-related markers (p < 0.001 vs. Tz). In conclusion, taurine exerts a potent hepatoprotective effect against tartrazine-induced liver injury, likely through SIRT-1 upregulation and HMGB-1 pathway inhibition, thereby reducing oxidative stress, inflammation, and fibrogenesis.