Abstract
Sutherlandia frutescens (L.) R.Br. (SF) is a medicinal plant indigenous to southern Africa and used in folk and contemporary remedies for stress, chronic diseases, cancer, and HIV/AIDS. While previous studies have focused on physiological effects of SF on cellular and systemic abnormalities associated with these diseases, little is known about its effects in the brain and immune cells in the central nervous system. Results of this study indicate that ethanol extracts of SF (SF-E) suppress NMDA-induced reactive oxygen species (ROS) production in neurons, and LPS- and IFNγ-induced ROS and nitric oxide (NO) production in microglial cells. SF-E’s action on microglial cells appears to be mediated through inhibition of the IFNγ-induced p-ERK1/2 signaling pathway which is central to regulating a number of intracellular metabolic processes including enhancing STAT1α phosphorylation and filopodia formation. The involvement of SF in these pathways suggests the potential for novel therapeutics for stress and prevention, and/or treatment of HIV/AIDS as well as other inflammatory diseases in the brain.
Highlights
Sutherlandia frutescens (SF) has long been used as a traditional medicinal plant in southern Africa for treatment of cancer, as well as a variety of chronic ailments, and more recently, HIV/AIDS [1,2,3]
We demonstrate that ethanol extracts of Sutherlandia frutescens (SF-E) mitigate N-methyl-D-aspartic acid (NMDA)-induced neuronal oxidative responses and LPSand cytokine-induced inflammatory responses in microglial cells
Based on earlier work indicating that NMDA, the ionotropic glutamatergic receptor agonist, stimulates rapid production of reactive oxygen species (ROS) in neurons through activation of NADPH oxidase [19], several studies have demonstrated that botanical polyphenols such as EGCG from green tea as well as honokiol and magnolol from magnolia bark suppress this ROS pathway [25,26]
Summary
Sutherlandia frutescens (SF) has long been used as a traditional medicinal plant in southern Africa for treatment of cancer, as well as a variety of chronic ailments, and more recently, HIV/AIDS [1,2,3]. Limited studies suggest multiple actions of SF as a consequence of putative antioxidant and anti-inflammatory activities [4,5,6,7,8], including inhibition of phorbol ester-induced COX-2 expression in human breast epithelial cells and mouse skin [6,7]. Neuroinflammation is known to play a major role in the progression of neurodegenerative diseases such as Alzheimer’s and Parkinson’s diseases, stroke, and HIV/AIDS encephalopathy [10,11]. Microglial activation is associated with the release of reactive oxygen species (ROS), nitric oxide (NO), glutamate, cytokines, phospholipases and proteases [13,14,15,16], factors contributing to the progressive neuronal damage observed in many neurodegenerative disorders. Suppressing or limiting microglial activation can have beneficial effects for preventing neuroinflammation and neurodegeneration
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