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Neuroprotective effects of curcumin-loaded nanophytosome on ketamine-induced schizophrenia-like behaviors and oxidative damage in male mice.

A. Hajizadeh Moghaddam, Khadijeh Maboudi, Bita Bavaghar, Seyed Reza Mokhtari Sangdehi, M. Zare

Neuroscience Letters September 15, 2021 DOI: 10.1016/j.neulet.2021.136249 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Preclinical study Peer reviewed
Population Mice
Interventions Curcumin Curcumin-loaded nanophytosome (CNP)
Dose 20 mg/kg
Duration 30 days
Measures forced swimming test (FST), open field test (OFT), novel object recognition test (NORT)
Topics Esketamine Ketamine
Key points Curcumin-loaded nanophytosome (CNP) had greater neuroprotective effects than free curcumin against ketamine-induced behavioral deficits and oxidative stress in mice.

Abstract

Curcumin as an antioxidant natural herb has shown numerous pharmacological effects. However, the poor bioavailability of curcumin is a significant pharmacological barrier for its antioxidant activities. The present study was conducted to develop curcumin-loaded nanophytosome (CNP) and explore their therapeutic potential in a ketamine (KET)-induced schizophrenia (SCZ) model. The mice in our experiment were treated orally with curcumin and CNP (20 mg/kg) for 30 consecutive days. In addition, the animals received intraperitoneal injection of KET (30 mg/kg/day) from the 16th to the 30th day. SCZ-like behaviors were evaluated employing forced swimming test (FST), open field test (OFT), and novel object recognition test (NORT), and oxidative stress markers in the brain were estimated. Our results revealed that CNP has a greater neuroprotective effect compared to free curcumin. CNP pretreatment significantly ameliorated KET-induced brain injury evidenced by a marked reduction in the depressive and anxiety-like behaviors, memory deficits, and oxidative stress markers in cortical and subcortical tissues. Therefore, CNP, as a suitable drug delivery system, may improve curcumin bioavailability and confer stronger neuroprotective effects against KET-induced behavioral deficits and oxidative damages.