ArticleInflammopharmacology2019
Targeting oxidative stress, acetylcholinesterase, proinflammatory cytokine, dopamine and GABA by eucalyptus oil (Eucalyptus globulus) to alleviate ketamine-induced psychosis in rats.
Article in Inflammopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 20 citations in OpenAlex.
- Sertraline and Escitalopram But Not Other Antidepressants Increase Acetylcholinesterase ActivityAnnals of neurosciences · 2026Article
- Effects ofBiochemistry and biophysics reports · 2024Article
- Pharmacological screening of silibinin for antischizophrenic activity along with its acute toxicity evaluation in experimental animals.Frontiers in pharmacology · 2023Article
- Natural essential oils derived from herbal medicines: A promising therapy strategy for treating cognitive impairment.Frontiers in aging neuroscience · 2023Review
- Forest Biomass as a Promising Source of Bioactive Essential Oil and Phenolic Compounds for Alzheimer's Disease Therapy.International journal of molecular sciences · 2022Review
- Study of Neuroprotection by a Combination of the Biological Antioxidant (Molecules (Basel, Switzerland) · 2021Article
- Potential Nutraceutical Properties of Leaves from Several Commonly Cultivated Plants.Biomolecules · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Essential oil of eucalyptus species is among the most common traded essential oils in the world. There is an increasing interest in the application of eucalyptus oil as a natural additive in food and pharmaceutical industry. The present study was undertaken to identify the phytoconstituents present in the essential oil of Eucalyptus globulus leaves (EO) and ascertain their protective effect against ketamine-induced psychosis in rats. GC-MS technique was used for analysis of phytoconstituents present in EO. Ketamine (50 mg/kg, i.p.) was used to induce psychosis in rats. Photoactometer, forced swim test and pole climb avoidance test were used to evaluate the protective effects of the EO (500, 1000 and 2000 mg/kg, p.o.) on acute and chronic administration. Bar test was used to test the side effect of EO. Biochemical and neurochemical estimations were carried out to explore the possible mechanism of action. GC-MS analysis of EO showed the presence of a number of biologically active compounds. EO at the dose of 500, 1000 and 2000 mg/kg, p.o. on acute and chronic administration, decreased locomotor activity, immobility duration and latency to climb the pole. EO was effective to facilitate the release of GABA, increase GSH levels, inhibit dopamine neurotransmission and decrease TNF-α levels as well as diminish AChE activity in different regions of the brain. EO at the dose of 500, 1000 mg/kg did not produce cataleptic behavior in rats. EO at the dose of 500, 1000 mg/kg produced protective effects against ketamine-induced psychosis and can be further explored clinically against neuropsychiatric disorders.
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