Investigation on the mechanistic approach of trigonelline action in attenuating nitrosodiethylamine instigated rodent experimental liver injury

Abstract Background 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 ml/kg b.wt of 1% NDEA); (3), NDEA and Trigonelline (10 ml/kg b.wt of 1% NDEA + 50 mg kg -1 b.wt) supplemented; (4), Trigonelline. Alkaline phosphatase, aspartate aminotransferase, alanine transaminase, bilirubin, serum nitrite estimation, protein carbonylation, Ca 2+ /Mg 2+ -ATPases, superoxide dismutase and malondialdehyde were examined. Haematoxylin-Eosin staining and scanning electron microscopy was used to monitor anatomical changes. Results NDEA perturbs liver function enzymes ALP, ALT, AST and bilirubin and, augmented levels of sera nitrites, protein carbonyls, lipid peroxides. Noticeable decline in Ca 2+ /Mg 2+ -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. Conclusion Hepatoprotection confered by TG is achieved through neutralizing free radicals via promoting a coupling reaction of free radicals to form stable products to exert protective effect against NDEA-induced liver injury.