Affiliations: [a] Department of Pharmacy Practice and Pharmacotherapeutics, University of Sharjah, Sharjah, UAE
| [b] Department of Clinical Pharmacy, Jordan University of Science and Technology, Irbid, Jordan
| [c] Department of Applied Biology, Jordan University of Science and Technology, Irbid, Jordan
| [d] Department of Biotechnology and Genetic Engineering, Jordan University of Science and Technology, Irbid, Jordan
| [e] Department of Pharmacology, Faculty of Medicine, Jordan University of Science and Technology, Irbid, Jordan
Correspondence:
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Corresponding author: Karem H. Alzoubi, Department of Pharmacy Practice and Pharmacotherapeutics, University of Sharjah, Sharjah, UAE. Tel.: +971 6 5057077; Fax: +971 6 5057078; E-mail: kelzubi@sharjah.ac.ae.
Abstract: Background: Post-traumatic stress disorder (PTSD) is a genuine obstructing mental disorder. As indicated by the name, it is related to the patients’ stress augmented by life-threatening conditions or accidents. The PTSD has linked to oxidative stress that can result in neurodegeneration. L-carnitine (L-CAR) is known for its antioxidant properties, which can protect against neuronal damage. Objective: In the current study, we investigated the beneficial effects of L-CAR on the memory impairment induced by PTSD using a rat model. Methods: A model of single-prolonged stress (a cycle of restraining, forced swimming, rest, and finally diethyl ether exposure for 2 h, 20 min, 15 min, and 1–2 min, respectively) was used to induce PTSD-like behavior. Intraperitoneal L-CAR treatment (300 mg/kg/day) was introduced for four weeks. Both memory and special learning were evaluated utilizing the radial arm water maze (RAWM). Moreover, the levels of glutathione peroxidase (GPx), glutathione reduced (GSH), and glutathione oxidized (GSSG) were assessed as biomarkers oxidative stress in the hippocampus. Results: The results demonstrated that both the short and long-term memories were impaired by PTSD/SPS model (P < 0.05), while L-CAR treatment prevented this memory impairment in PTSD rats. Besides, L-CAR prevented the reduction in GPx activity and increase in GSSG, which were altered in the hippocampus of the PTSD/SPS rats (P < 0.05). Levels of GSH were not changed in PTSD and/or L-CAR rats. Conclusions: L-CAR administration prevented short- and long-term memories’ impairments induced in the PTSD/SPS rat model. This is probably related to its antioxidant effects in the hippocampus.
