Abstract
Microglia respond to adverse stimuli in order to restore brain homeostasis and, upon activation, they release a number of inflammatory mediators. Chronic microglial overactivation is related to neuroinflammation in Alzheimer’s disease. In this work, we show that oleanolic acid (OA), a natural triterpene present in food and medicinal plants, attenuates the activation of BV2 microglial cells induced by lipopolysaccharide (LPS). Cell pretreatment with OA inhibited the release of IL-1β, IL-6, TNF-α, and NO, which was associated with the downregulation of the expression of genes encoding for these cytokines and inducible nitric oxide synthase (iNOS), and the reinforcement of the endogenous antioxidant cell defense. These findings advocate considering OA as a novel neuroprotective agent to inhibit oxidative stress and inflammatory response in activated microglia associated with Alzheimer’s disease.
Highlights
In 2017, between 45 and 50 million individuals suffered from Alzheimer’s disease (AD), and it is expected that the prevalence of the disease will quadruple by 2050
Cell viability was not threatened by the presence of oleanolic acid (OA) concentrations lower than 10 μM, a range in which the proportion of active cells always remained above 85%
We investigated the effect of OA on nitric oxide (NO) production, which is regulated by inducible nitric oxide synthase (iNOS) activity
Summary
In 2017, between 45 and 50 million individuals suffered from Alzheimer’s disease (AD), and it is expected that the prevalence of the disease will quadruple by 2050. AD, the most common form of dementia, is characterized pathologically by a substantial neuronal and synaptic loss, chronic inflammation, and a decrease in cognitive abilities [1]. The causes of AD are not fully understood, but it is well known that abnormal deposits of amyloid-β (Aβ) and neurofibrillary aggregates of hyperphosphorylated tau protein occur in the cerebral cortex [2]. These events worsen with age, and include inflammation, oxidative stress, and mitochondrial dysfunction [3,4]. Extravasation of circulating neuroinflammatory molecules may increase the onset risk and worsen the development of the disease [5]
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