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Review
. 2022;20(11):2156-2174.
doi: 10.2174/1570159X20666220119140835.

Neuroinflammation: The Role of Anthocyanins as Neuroprotectants

Otilia J F Banji  1 , David Banji  2 , Hafiz A Makeen  1 , Saad S Alqahtani  1 , Saeed Alshahrani  2
Affiliations
Review

Neuroinflammation: The Role of Anthocyanins as Neuroprotectants

Otilia J F Banji et al. Curr Neuropharmacol. 2022.

Abstract

Neuroinflammation is a trigger for several neurodegenerative and neuropsychiatric disorders. Exposure to noxious external stimuli induces homeostatic disturbances resulting in morphological changes in microglia, their activation, and elaboration of pro-inflammatory mediators. This leads to neuroinflammation with the progressive loss of neurons. Nutraceuticals such as anthocyanins are a class of brightly colored bioactive compounds present in fruits and vegetables with purported health benefits. They interfere with the activation of several signaling cascades that have a prominent role in preventing neuroinflammation. More importantly, anthocyanins can cross the blood-brain barrier and are safe. Hence, the current review focuses on the bioavailability of anthocyanins, clinical and in vitro evidence on their role in impeding the activation of transcription factors, modulating the immune milieu within the central nervous system, preventing the activation of microglia, and averting neuroinflammation.

Keywords: Anthocyanins; bioavailability; microglia; neuroinflammation; oxidative stress; signaling pathways.

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Figures

Fig. (1)
Fig. (1)
Bioaccessibility of anthocyanins and their passage across several barriers.
Fig. (2)
Fig. (2)
Metabolism and metabolites formed from anthocyanins. Cy3G: Cyanidin-3-glucoside.
Fig. (3)
Fig. (3)
Anthocyanins and their impact on NFkB signaling. Anthocyanins exert their action on various sites of the NFkB pathway. The activation of Toll-like receptors (TLR), and RAGE (Receptor for advanced glycation end products) is blocked. Also, anthocyanins suppress IKK kinase, prevent the activation of p65, interfere with the nuclear translocation of NF-κB and the expression of pro-inflammatory factors that are responsible for neuroinflammation.
Fig. (4)
Fig. (4)
Role of anthocyanins in alleviating oxidative stress-mediated neuroinflammation. Anthocyanins target ASK1 and prevent activation of the MAPK (Mitogen-activated protein kinases), JNK (c-Jun N-terminal kinases), and ERK (extracellular signal-regulated kinase) pathways. Activation of AP-1 and NFκB is attenuated. In addition, anthocyanins also affect the activation of PI3K/Akt pathway and prevent the activation of NFκB. Abbreviations: ASK1: Apoptosis signal regulating kinase 1; AP-1: Activator protein-1; Mitogen-activated protein kinases kinase (MEKK, MKK3, MKK4, MKK7; NFκB: Nuclear factor-kappa B; PIP2: phosphatidylinositol-4,5-bisphosphate; PIP3: phosphatidylinositol-3,4,5-bisphosphate PI3K: phosphatidylinositol 3-kinase; Akt: Protein kinase B; GSK2B: Glycogen synthase kinase 3 beta.
Fig. (5)
Fig. (5)
Molecular sites of action of anthocyanins. Anthocyanins have a multifaceted role by exerting an action on receptors, signaling pathways and enzymes. The activation of transcription factors and the expression of pro-inflammatory cytokines is blocked.
See this image and copyright information in PMC

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