Abstract
In recent years, microalgae have drawn increasing attention as a valuable source of functional food ingredients. Intriguingly, Nitzschia laevis is rich in fucoxanthinol that is seldom found in natural sources. Fucoxanthinol, a marine xanthophyll carotenoid, possesses various beneficial bioactivities. Nevertheless, it’s not clear whether fucoxanthinol could exert anti-neuroinflammatory function. In light of these premises, the aim of the present study was to investigate the anti-inflammatory role of fucoxanthinol purified from Nitzschia laevis in Lipopolysaccharide (LPS)-stimulated microglia. The results showed that pre-treatment of fucoxanthinol remarkably attenuated the expression of LPS-induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and the production of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), prostaglandin E2 (PGE-2), nitric oxide (NO) and reactive oxygen species (ROS) induction. Modulation mechanism studies revealed that fucoxanthinol hampered nuclear factor-kappa B (NF-κB), Akt, and mitogen-activated protein kinase (MAPK) pathways. Meanwhile, fucoxanthinol led to the enhancement of nuclear translocation of NF-E2-related factor 2 (Nrf2), and the upregulation of heme oxygenase-1 (HO-1) and NAD(P)H: quinone oxidoreductase 1 (NQO-1). Taken together, the results indicated that fucoxanthinol obtained from Nitzschia laevis had great potential as a neuroprotective agent in neuroinflammation and neurodegenerative disorders.
Highlights
IntroductionThe principal primary resident macrophages in the central nervous system (CNS), occupy a pivotal role in the neuroinflammatory responses as well as homeostatic maintenance [1]
Microglia, the principal primary resident macrophages in the central nervous system (CNS), occupy a pivotal role in the neuroinflammatory responses as well as homeostatic maintenance [1].In the normal state, microglia serve as phagocytes and function in host protection of the brain [2].aberrantly activated microglia can bring about the release of various pro-inflammatory cytokines and mediators, including nitric oxide (NO), prostaglandin E2 (PGE-2), reactive oxygen species (ROS), interleukin (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α), which are closely related to neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, Huntington’s disease, and stroke [3,4,5,6]
Aberrantly activated microglia can bring about the release of various pro-inflammatory cytokines and mediators, including nitric oxide (NO), prostaglandin E2 (PGE-2), reactive oxygen species (ROS), interleukin (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α), which are closely related to neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, Huntington’s disease, and stroke [3,4,5,6]
Summary
The principal primary resident macrophages in the central nervous system (CNS), occupy a pivotal role in the neuroinflammatory responses as well as homeostatic maintenance [1]. Aberrantly activated microglia can bring about the release of various pro-inflammatory cytokines and mediators, including nitric oxide (NO), prostaglandin E2 (PGE-2), reactive oxygen species (ROS), interleukin (IL-1β), IL-6, and tumor necrosis factor-alpha (TNF-α), which are closely related to neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), multiple sclerosis, Huntington’s disease, and stroke [3,4,5,6]. Impeding the aberrant activation of microglia is considered an effective therapeutic option for the treatment of neuro-inflammation-related diseases. Nuclear factor-kappa B (NF-κB), a critical transcription factor in modulating microglia-mediated inflammation, consists of P50, P65, and IκB.
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