Ginger mitigates acrylamide-induced hepatotoxicity through antioxidant and anti-inflammatory mechanisms in rats

Figure 1 Effect of treatments. A: Liver enzymes [alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP)]. The graph shows a marked elevation in liver enzymes (ALT, AST, ALP) in the acrylamide (ACR)-treated group, indicating hepatocellular damage. Co-treatment with ginger significantly reduced enzyme levels, suggesting a protective effect. No significant difference was found between ginger alone and control groups; B: Oxidative stress markers [malondialdehyde (MDA), glutathione, catalase, superoxide dismutase]. Oxidative stress markers reveal increased lipid peroxidation and reduced antioxidant activity in the ACR group. Ginger significantly restored antioxidant levels and reduced MDA, indicating its antioxidant and protective potential. ^aP < 0.05 vs control, ^bP < 0.01 vs control, ^cP < 0.05 vs ACR group. ACR: Acrylamide; ALP: Alkaline phosphatase; ALT: Alanine aminotransferase; AST: Aspartate aminotransferase; CAT: Catalase; GSH: Glutathione; MDA: Malondialdehyde; SOD: Superoxide dismutase.

Figure 2 Histopathological examination of liver tissue in control and experimental groups. A: Control group showing normal central vein (black arrow) and normal hepatocytes (white arrow). The liver tissue shows no significant pathological alterations; B: Ginger treated group showing normal hepatocytes (white arrow), blood sinusoids between hepatocyte cords (black arrow); C: Acrylamide (ACR) treated group showing dilated and congested portal veins (black arrow) and blood sinusoids (white arrow), and hepatocytes with dark nucleus and vacuolated cytoplasm; D: ACR + ginger treated group showing moderate damage with mild dilated central veins (black arrow) (hematoxylin and eosin 200 ×).