Prevention of dimethyl hydrazine-induced liver damage by β-caryophyllene in rats

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Purpose: To investigate the hepato-protection of beta-caryophyllene (BCP) in rats exposed to 1,2-dimethylhydrazine (DMH). Methods: Sixty male Sprague-Dawley rats were distributed into six cohorts and administered 0.5 mL distilled water, 20 mg/kg DMH, 5 mg/kg BCP, 10 mg/kg BCP, 20 mg/kg DMH + 5 mg/kg BCP, and 20 mg/kg DMH + 10 mg/kg BCP. Liver damage was induced by weekly intraperitoneal DMH administration for 20 weeks, with once daily oral BCP treatment. After treatment, the rats were sacrificed, after which liver function markers, oxidative stress markers, and trace metals were assessed in blood and liver. The liver DNA fragmentation and histopathology were also determined. Results: The DMH-treated group exhibited significant elevations of alanine transaminase, aspartate transaminase, malondialdehyde, and glutathione-S-transferase (p < 0.05), coupled with significant decreases in hepatic superoxide dismutase, catalase, and glutathione peroxidase (p < 0.05). The DMH perturbed hepatic trace metal homeostasis by significantly reducing Ca, Cu, and Zn levels (p < 0.05), while Fe was markedly raised (p < 0.05). A higher frequency of DNA fragments, portal inflammation, and hepatocellular necrosis was found in DMH-treated group. However, co-treatment with BCP led to a remarkable restoration of the markers to near-control values and prevented DMH-induced lesions. Conclusion: These findings demonstrate that the preventive action of beta-caryophyllene is related to modulation of antioxidant defenses, metal homeostasis, and apoptosis.

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