LAVENDER ESSENTIAL OIL IMPROVED DEPRESSIVE BEHAVIOR IN MICE AFTER INTERFERON-α ADMINISTRATION BUT NOT AFTER CYCLOSPORINE A ADMINISTRATION

Document Type : Original Article

Authors

1 Department of Pharmacology and Toxicology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran

2 Isfahan Pharmaceutical Sciences Research Center, Department of Pharmacology and Toxicology, School of Pharmacy and Pharmaceutical Sciences, Isfahan University of Medical Sciences, Isfahan, Iran

Abstract

The purpose of this study was to assess whether Lavender essential oil (Lav) could alleviate depressive symptoms induced by Interferon-α (IFN-α) therapy, which reduces tryptophan levels, or Cyclosporine A (Cyc) treatment that leads to psychological issues by inhibiting the mammalian target of rapamycin (mTOR) receptor. The study focused on mice as the subjects for evaluation.  Lav 50,100,200 mcL/kg, and Cyc 40 mg/kg (all IP) and IFN-α 1600000 IU/kg SC were administered. The tests were performed after 6 days of consecutive injections on day 7. First total activity was evaluated by the locomotor test, following the splash test and then immobility time during the forced swimming test (FST) was measured. Sucrose preference was measured in order to test anhedonia. The selected treatments did not cause noticeable changes on the locomotor activity. IFN-α increased the immobility time during FST (178.6±10.4 s vs. control 125.8±17.7 s; P < 0.05) indicating depressive-like effect, and IFN-α-lav200 decreased it to (83.3±22.2 s, vs. IFN-α; P<0.01). The grooming time during splash test increased from 36.8±6.1s in IFN-α group to 106.3±9.6 in IFN-α-lav200 group (P<0.05). Sucrose preference increased to 82% following IFN-α-Lav200 administration. However, Lav did not cause a significant change on Cyc-induced depression. Conclusion: While Lav demonstrated a beneficial effect in mitigating IFN-α-induced depression in mice, it was not able to fully reverse Cyc-induced depression. This suggests that Lav exerts its antidepressant effects through distinct mechanisms that may not involve modifications to the mTOR pathways.

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