Abstract Title:

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

Abstract Source:

Naunyn Schmiedebergs Arch Pharmacol. 2020 Apr 17. Epub 2020 Apr 17. PMID: 32303785

Abstract Author(s):

Fatemeh Zare Mehrjerdi, Somayeh Niknazar, Maryam Yadegari, Fatemeh Ali Akbari, Zeynab Pirmoradi, Mehdi Khaksari

Article Affiliation:

Fatemeh Zare Mehrjerdi


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 significantlyrestored 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.

Study Type : Animal Study

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