RESUMO
Cyanobacterium Nostoc commune has long been used to alleviate various diseases. This research examines the effects of Nostoc commune extract (NCE) against behavioral disorders, cerebral oxidative stress, and inflammatory damage in the ketamine-induced schizophrenia model. Oral NCE administration (70 and 150 mg/kg/d) is performed after intraperitoneal ketamine injection (20 mg/kg) for 14 consecutive days. The forced swimming and open field tests are used to assess schizophrenia-like behaviors. After the behavioral test, dopamine (DA) level, oxidative stress markers, as well as the interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) expression are measured in the cerebral cortex. The results show that NCE treatment ameliorates KET-induced anxiety and depressive-like behaviors in OFT and FST, respectively. NCE considerably decreases the malondialdehyde (MDA) and DA levels and IL-6 and TNF-α expressions in mice with schizophrenia-like symptoms. Also, a significant increase is observed in the glutathione (GSH) level and catalase (CAT), superoxide dismutase (SOD), and glutathione reductase (GRx) activity in cerebral tissue. The present study shows that NCE treatment effectively improves KET-induced schizophrenia-like behaviors and oxidative and inflammatory damage. Therefore, NCE, via its bioactive constituents, could have strong neuroprotective effects in the schizophrenia-like model.
RESUMO
Schizophrenia (SCZ) is a profound neurological disorder that affects approximately 1% of the global population. Alpha-pinene (α-pinene) is a natural and active monoterpene found in coniferous tree oil, primarily pine, with diverse pharmacological characteristics, including antioxidative, anxiolytic, and antidepressant properties. This research study delves into the neuroprotective effects of α-pinene on oxidative stress, memory deficits, and depressive and anxiety-like behaviors in a ketamine-induced mice model of SCZ using male mice. The mice were randomly divided into six groups: vehicle, control, positive control, ketamine, α-pinene at 50 mg/kg, and α-pinene at 100 mg/kg. Treatment of the ketamine-induced mice model of SCZ with α-pinene yielded significant improvements in depressive and anxiety-like behaviors and cognitive impairments. Furthermore, it significantly elevated glutathione (GSH) levels, total antioxidant capacity (TAC), dopamine levels, catalase (CAT), and superoxide dismutase (SOD) activities while markedly reducing malondialdehyde (MDA) levels. The current study establishes that α-pinene treatment effectively mitigates oxidative damage, cognitive deficits, and depressive and anxiogenic-like behaviors in the brains of ketamine-treated mice. Therefore, α-pinene treatment is an efficacious approach to forestall the neurobehavioral and neurobiochemical adverse effects of the ketamine-induced SCZ model of mice.