4.7 Article

Microalgae extract induces antidepressant-like activity via neuroinflammation regulation and enhances the neurotransmitter system

Journal

FOOD AND CHEMICAL TOXICOLOGY
Volume 170, Issue -, Pages -

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.fct.2022.113508

Keywords

Botryococcus terribilis; Me-meijicoccene; Depression; Neuroinflammation; Neurotransmitter

Funding

  1. Tokyo Electric Power Company Holdings, Inc., Japan
  2. Japan Science and Technology Agency (JST), Science and Technology Research Partnership for Sustainable Development, Japan (SATREPS) [JPMJSA1506]

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The increasing prevalence of mental disorders, such as depression, is a serious public health concern. Microalgae, which contain various bioactive compounds, have been found to exhibit health benefits such as antioxidative, anti-inflammatory, anticancer, and anti-obesity effects. This study focused on the microalgal extract (ME) from Botryo-coccus terribilis and found that it ameliorated dexamethasone-induced cytotoxicity and induced antidepressant-like activity in stressed mice. ME was also found to regulate neuro-inflammation and modulate neurotransmitter systems, suggesting its potential in the treatment of depressive disorders.
The increasing prevalence of mental disorders, such as depression, is currently a serious public health concern. Microalgae are a diverse group of organisms that contain many bioactive compounds such as polyunsaturated fatty acids and polyphenols. These compounds can exhibit many health benefits such as antioxidative, anti-inflammatory, anticancer, and anti-obesity effects. In the present study, we focused on microalgal (Botryo-coccus terribilis) extract (ME) rich in Me-meijicoccene (MM), a novel compound. Our results showed that pre-treatment of SH-SY5Y cells with ME and MM ameliorated dexamethasone (depression-causing substance) -induced cytotoxicity. The results of the tail suspension test (TST) indicated that ME (50 mg/kg) induced antidepressant-like activity in TST-stressed mice. Our microarray analysis revealed that ME upregulated neurotransmitter-related gene (neurotransmitter secretion) expression and downregulated neuroinflammatory-related gene (chemokine-mediated signaling) expression in the cerebral cortex. ME also induced an increase in neurotransmitter and brain-derived neurotrophic factor levels, and a decrease in corticosterone and pro -inflammatory cytokine levels in the serum, cerebral cortex, and hypothalamus. Altogether, our study is the first to report that 50 mg/kg ME (not 100 mg/kg) exerts antidepressant-like effects via regulating neuro-inflammation and modulating neurotransmitter systems in the mouse brain, highlighting the prospects of ME in the treatment of depressive disorders of a psychosocial nature.

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