Effects of Nostoc commune extract on the cerebral oxidative and neuroinflammatory status in a mice model of schizophrenia
Parisa Jahani Bahnamiri, Akbar Hajizadeh Moghaddam, Mojtaba Ranjbar, Ehsan Nazifi
Biochemistry and Biophysics Reports December 8, 2023 DOI: 10.1016/j.bbrep.2023.101594 via DOAJ
Summary
AI-generated from the abstractAn extract from the cyanobacterium Nostoc commune (NCE) given orally to mice at 70 or 150 mg/kg per day for 14 days reduced anxiety- and depression-like behaviors caused by ketamine, a model of schizophrenia. In the cerebral cortex, NCE lowered dopamine levels, reduced the oxidative stress marker malondialdehyde, and decreased the inflammatory cytokines IL-6 and TNF-α. It also increased the antioxidant glutathione and the activity of catalase, superoxide dismutase, and glutathione reductase. The findings suggest that NCE may protect the brain from schizophrenia-like behavioral, oxidative, and inflammatory damage.
Study at a glance
| Characteristics | Animal experimental study Peer reviewed |
|---|---|
| Population | Mice with ketamine-induced schizophrenia-like symptoms |
| Intervention | Nostoc commune extract |
| Dose | 70 and 150 mg/kg/d |
| Duration | 14 consecutive days |
| Topics | Ketamine |
| Keywords | Nostoc commune Schizophrenia Oxidative damages Inflammatory cytokines |
| Citations | 3 |
| Key finding | Nostoc commune extract reduced anxiety- and depressive-like behaviors and lowered oxidative stress and inflammatory markers in the cerebral cortex of mice with ketamine-induced schizophrenia-like symptoms. |
Abstract
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.