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Carvacrol reduces hippocampal cell death and improves learning and memory deficits following lead-induced neurotoxicity via antioxidant activity

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Abstract

Carvacrol is a monoterpene with neuroprotective effects in several animal models of neurodegeneration, including epilepsy, ischemia, and traumatic neuronal events. In this study, we aimed to examine the effects of carvacrol on neurodegeneration induced by lead acetate in rats. A total of 50 male Wistar rats were divided into five equal groups. The control group received drinking water, while the neurotoxic group was exposed to 500 ppm of lead acetate in drinking water for 40 days. The three remaining groups, which were also exposed to 500 ppm of lead acetate, received carvacrol at doses of 25, 50, and 100 mg/kg orally for 40 days. The Morris water maze test was employed to examine spatial learning and memory. Pathological damage to the hippocampus was determined by Nissl staining. The level of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT) were detected using biochemical analysis and the free radical scavenging activity as evaluated by the DPPH test. Administration of carvacrol significantly restored learning and memory impairment induced by lead acetate. Moreover, carvacrol ameliorated neurodegeneration, antioxidative capacity, and lipid peroxidation in the hippocampus of rats exposed to lead. The present results provide a rationale for the inhibitory role of carvacrol in the attenuation of lead-induced neurotoxicity.

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Funding

This study was supported by grant No: 5458 from the Neurobiomedical Research Center, School of Medicine, Shahid Sadoughi University of Medical Sciences and Health Services.

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Contributions

FZ and MK conceived and designed the research; SN, MY, FA, and ZP conducted the experiments and analyzed the data. FA and ZP conducted viability experiments and analyzed the data. FZ, MK, SN, and MY interpreted results. FZ, MK, and MY wrote the manuscript. All the authors read and approved the manuscript.

Corresponding author

Correspondence to Mehdi Khaksari.

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Conflict of interest

No potential conflict of interest was reported by the authors.

Ethical approval

All procedures were performed in accordance with the National Institutes of Health Guidelines for the Care and Use of Laboratory Animals and were approved in the ethics committee (IR.SSU.MEDICINE.REC.1396.317).

The experimental investigation we would have wished to perform, in order to further and convincingly support the unprecedentedly strong effects of carvacrol, would be a blinded qPCR analysis of catalase and SOD transcription in lysates of all frozen animal brains. However, this was not possible for us, as economic sanctions that are in effect on us from outside of the scientific arena, unfortunately, made such investigations impossible. We will immediately catch up with such confirmation testing as soon as routine qPCR analysis will again be doable for us.

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Zare Mehrjerdi, F., Niknazar, S., Yadegari, M. et al. Carvacrol reduces hippocampal cell death and improves learning and memory deficits following lead-induced neurotoxicity via antioxidant activity. Naunyn-Schmiedeberg's Arch Pharmacol 393, 1229–1237 (2020). https://doi.org/10.1007/s00210-020-01866-6

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  • DOI: https://doi.org/10.1007/s00210-020-01866-6

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