Abstract
In this study, we aimed to evaluate the antioxidant and anti-inflammatory properties of Opuntia ficus-indica cactus cladode extracts in microglia BV-2 cells. Inflammation associated with microglia activation in neuronal injury can be achieved by LPS exposure. Using four different structurally and biologically well-characterized LPS serotypes, we revealed a structure-related differential effect of LPS on fatty acid β-oxidation and antioxidant enzymes in peroxisomes: Escherichia coli-LPS decreased ACOX1 activity while Salmonella minnesota-LPS reduced only catalase activity. Different cactus cladode extracts showed an antioxidant effect through microglial catalase activity activation and an anti-inflammatory effect by reducing nitric oxide (NO) LPS-dependent production. These results suggest that cactus extracts may possess a neuroprotective activity through the induction of peroxisomal antioxidant activity and the inhibition of NO production by activated microglial cells.
Highlights
Excessive oxidative stress triggered by the generation of reactive oxygen species (ROS) has been linked to aging, neuroinflammation and neurodegenerative diseases such as Alzheimer disease, multiple sclerosis and peroxisomal leukodystrophies [1]
We have recently shown down-regulation of genes involved in hepatic peroxisomal fatty acid oxidation (FAOx) in mice exposed to LPS [22]
Murine microglial BV-2 cell lines (BV-2) were grown in a 5% CO2 incubator at 37 °C in Dulbecco’s modified Eagle medium (DMEM) supplemented with 10% (v/v) heat inactivated fetal bovine serum (FBS) and 1% antibiotics; culture medium was changed
Summary
Excessive oxidative stress triggered by the generation of reactive oxygen species (ROS) has been linked to aging, neuroinflammation and neurodegenerative diseases such as Alzheimer disease, multiple sclerosis and peroxisomal leukodystrophies [1]. Microglia plays a central role in the neuroinflammation and in the physiopathogenesis of these disorders by producing proinflammatory molecules, such as tumor necrosis factor-α (TNF-α), interleukin-1 and 6, and nitric oxide (NO) [2,3,4]. Generation of ROS by LPS-activated microglia plays a key role in the triggered neurotoxicity [9], which can be largely reduced by neutralizing the extracellular hydrogen peroxide and superoxide by catalase and superoxyde dismutase treatment respectively [10,11]. Such results underlined the antioxidant role of peroxisomal proteins, catalase
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