Background: Drug-induced acute liver damage is a contributing factor in nearly 50% of acute liver failures. Acute liver failure has been linked to pharmaceutical overdoses, particularly with paracetamol. Plant-based medication could be a possible agent for mitigating the effects of paracetamol overdose. The present study investigated Pimenta dioica (PD) berries extract for its hepatoprotective properties against paracetamol-induced liver toxicity in rats. Materials and Methods: Two chemicals, paracetamol and silymarin, were used in this study. Furthermore, fully mature berries of PD were used to extract the bioactive constituents in 90% ethanol. Moreover, male Wistar albino rats (n = 40) were used to assess the hepatoprotective activity. For this purpose, hepatotoxicity was induced by orally administering 2 g/kg body weight of paracetamol. The rats were divided into five groups. Group I (control group) received 1 mL/kg of 1% sodium carboxymethyl cellulose. Group II (hepatotoxic control group) received an oral dose of 2 g/kg of paracetamol. Group III was given silymarin at a dose of 100 mg/kg. Group IV and V received PD at 200 mg/kg and 400 mg/kg, respectively. The liver was surgically excised to calculate relative liver weight and histopathological examination in different rat groups. Blood samples were collected from the retro-orbital plexus on the 8th day of treatment and examined for serum alkaline phosphatase (ALP), alanine transaminase (ALT), aspartate aminotransferase (AST), total bilirubin (TB) content, and gamma-glutamyl transferase (GGT) levels. The data were statistically analyzed using a one-way Analysis of Variance (ANOVA), with a p-value < 0.05 considered significant. Results: It was observed that paracetamol significantly increased (p < 0.001) relative liver weight as well as liver biomarker enzymes such as ALP, ALT, AST, TB, and GGT. Furthermore, paracetamol caused histological alterations in the hepatocytes. Moreover, Pimenta dioica (PD) significantly inhibited (p < 0.001) paracetamol-induced changes in relative liver weight, liver biomarkers levels, and hepatocyte histopathology in a dose-dependent manner. Conclusion: These findings suggest that PD possesses hepatoprotective properties against paracetamol-induced hepatocellular damage. Although, based on the current findings, it is difficult to speculate on the precise mechanism of action, attenuation of paracetamol-induced generation of free radicals could be one of the mechanisms. Therefore, further investigation to identify potentially active components and to establish the precise mechanism of action for its hepatoprotective effect could make PD a novel candidate for therapeutic use.