Abstract
Microglia are the macrophages that reside in the brain. Activated microglia induces further activation of astrocytes and neuronal cells for mounting an immune response. However, activated microglia release neurotoxic mediators causing neuroinflammation, which is associated with chronic etiology of neurodegenerative diseases. We investigated the effect of ethanol extract of Physalis alkekengi L. var. francheti fruit (PAFE) on neuronal cell death mediated by activated microglia. PAFE decreased NO production and IL-6 secretion in LPS-stimulated BV-2 and primary microglial cells without reducing cell viability. Consistently, treatment with PAFE decreased iNOS and COX-2 expression and ERK phosphorylation in LPS-stimulated BV-2 cells. Finally, apoptosis of N2a cells grown in conditioned media prepared from LPS-stimulated BV-2 cells containing PAFE was inhibited via downregulation of the Bax/Bcl-2 ratio. Taken together, PAFE alleviates neuronal cell death by reducing neurotoxic mediators such as NO and IL-6 from activated microglia. Therefore, it could be a potential candidate to treat neurodegenerative diseases caused by chronic neuroinflammation.
Highlights
Microglia are neurological macrophage that reside in the central nervous system and share tissue-specific primary immune functions linked to adaptive immune function [1, 2]
PAFE reduces nitric oxide (NO) generation in the BV‐2 cells activated by treating LPS Activated BV-2 microglia release NO as an inflammatory response
We observed that the production of nitrite, a soluble form of NO oxidation, decreased as the concentration of the PAFE increased beyond 1 μg/mL, suggesting that the PAFE inhibited NO generation in the BV-2 cells activated by LPS stimulation (Fig. 1a)
Summary
Microglia are neurological macrophage that reside in the central nervous system and share tissue-specific primary immune functions linked to adaptive immune function [1, 2]. Microglia are activated by external cues including lipopolysaccharide (LPS), β-amyloid, and interferon-γ, which are accompanied by an inflammatory response following the release of a group of mediators including nitric oxide (NO), IL-6, IL-1β, prostaglandin E 2, and TNF-α [3,4,5,6]. This secreted inflammatory mediators activate astrocytes, leading to further activation of microglia, forming amoeboid morphology with increased cell size for a protective role against threats [7,8,9]. We investigated the effect of PAF on the release of inflammatory mediators from LPS-stimulated microglia and its influence on neuroblastoma cell death
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