Background <p>Researches document a continued increase in liver diseases world over. Factors like obesity, alcohol, synthetic drugs, parasites/viruses, and nitrosamines are reported to contribute majority of liver diseases. It has been argued that oxidative stress plays a significant role in most of the liver damages. Conversely, the incessant use of synthetic medicines also exerts unnecessary burden on the liver. Therefore, there is a need to evaluate adequate alternatives to treat liver disorders efficiently. This study is aimed at evaluating the mechanism of N-Nitrosodiethylamine (NDEA) induced liver injury vis â vis amelioration of the disease by trigonelline. Four groups of rats (Wistar strain), three in each group were maintained: (1), saline control; (2), NDEA (single dose; 10&#xa0;ml/kg b.wt of 1% NDEA); (3), NDEA and Trigonelline (10&#xa0;ml/kg b.wt of 1% NDEA + 50&#xa0;mg kg^-1 b.wt) supplemented; (4), Trigonelline. Alkaline phosphatase, aspartate aminotransferase, alanine transaminase, bilirubin, serum nitrite estimation, protein carbonylation, Ca²⁺/Mg²⁺-ATPases, superoxide dismutase and malondialdehyde were examined. Haematoxylin-Eosin staining and scanning electron microscopy was used to monitor anatomical changes.</p> Results <p>NDEA perturbs liver function enzymes ALP, ALT, AST and bilirubin and, augmented levels of sera nitrites, protein carbonyls, lipid peroxides. Noticeable decline in Ca²⁺/Mg²⁺-ATPase and SOD activity was also recorded. Microscopy studies revealed gross architectural changes in the liver of NDEA-treated animals. However, TG significantly refurbished the liver protein biochemistry, oxidative stress biomarkers and cellular damage in the liver within two weeks.</p> Conclusion <p>Hepatoprotection confered by TG is achieved through neutralizing free radicals <i>via</i> promoting a coupling reaction of free radicals to form stable products to exert protective effect against NDEA-induced liver injury.</p>