Abstract
Neuroinflammation is involved in various neurological diseases. Activated microglia secrete many pro-inflammatory factors and induce neuronal cell death. Thus, the inhibition of excessive proinflammatory activity of microglia leads to a therapeutic effect that alleviates the progression of neuronal degeneration. In this study, we investigated the effect of Croton tiglium (C. tiglium) Linn. extract (CTE) on the production of pro- and anti-inflammatory mediators in microglia and astrocytes via RT-PCR, Western blot, and nitric oxide assay. Neurotoxicity was measured by cell viability assay and GFP image analysis. Phagocytosis of microglia was measured using fluorescent zymosan particles. CTE significantly inhibited the production of neurotoxic inflammatory factors, including nitric oxide and tumor necrosis factor-α. In addition, CTE increased the production of the neurotrophic factor, brain-derived neurotrophic factor, and the M2 phenotype of microglia. The culture medium retained after CTE treatment increased the survival of neurons, thereby indicating the neuroprotective effect of CTE. Our findings indicated that CTE inhibited pro-inflammatory response and increased the neuroprotective ability of microglia. In conclusion, although CTE is known to be a poisonous plant and listed on the FDA poisonous plant database, it can be used as a medicine if the amount is properly controlled. Our results suggested the potential benefits of CTE as a therapeutic agent for different neurodegenerative disorders involving neuroinflammation.
Highlights
Neuroinflammation is observed in many neurological disorders, including Alzheimer disease (AD), stroke, multiple sclerosis, Parkinson’s disease (PD), and neuroinfections [1,2,3]
CTE is known to be a poisonous plant and listed on the Food and Drug Administration (FDA) poisonous plant database, it can be used as a medicine if the amount is properly controlled
CTE significantly inhibited the production of neurotoxic inflammatory factors, including nitric oxide (NO) and tumor necrosis factor (TNF)-α
Summary
Neuroinflammation is observed in many neurological disorders, including Alzheimer disease (AD), stroke, multiple sclerosis, Parkinson’s disease (PD), and neuroinfections [1,2,3]. Inflammatory activation of microglia (called as proinflammatory M1 microglia) increases neuroinflammation by releasing proinflammatory factors, including nitric oxide (NO), prostaglandin. E2, tumor necrosis factor (TNF)-α, and interleukin (IL)-1β. These molecules are known to promote the progression of neurodegenerative diseases [4,5]. Alternatively activated microglia (called anti-inflammatory M2 microglia) have neuroprotective properties that release neurotrophic factors (nerve growth factor or brain-derived neurotrophic factor; BDNF) and eliminate abnormal protein aggregation and pathogens [6,7,8]. Efforts are underway to identify natural materials and their target molecules that inhibit M1 inflammatory activation and promote M2 activation, and can be used as therapeutic agents for neurological diseases
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