Regulation of chronic neuroinflammation through dietary herbal products

Abstract

Chronic neuroinflammation is a consequence of disease pathogenesis underlying neurological disorders at large. While the immune response that triggers inflammatory signaling cascades is unresolved, its progression could cause functional damage to neurons and glial cells, including astrocytes, microglia, and oligodendrocytes. Controlling neuroinflammatory signaling at the early stage of disease pathogenesis is critical to prevent irreversible tissue necrosis. While the application of anti-inflammatory drugs is standard practice, their protracted use is known to cause gastrointestinal injuries, further enhancing the risk of cardiovascular, renal, liver, and lung diseases. Several medicinal herbs and herbal products with anti-inflammatory potential could be effective substitutes. This review aims to identify the preclinical data from important dietary herbal products that have demonstrated anti-neuroinflammatory efficacy in several animal models. The reviewed dietary herbal products are sourced from Bacopa monnieri, Centella asiatica, Emblica officinalis, Piper nigrum, Zingiber officinale, Punica granatum, Mucuna pruriens, Clitoria ternatea, Moringa oleifera, Phoenix dactylifera and Curcuma longa. This review is based on emphatic data from these products demonstrating the significant anti-neuro-inflammatory potential that could probably reduce neuroinflammatory signaling in a neurological disorder and promote brain health and well-being. Abundant scientific evidence shows that critical proinflammatory cytokines in the brain, such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-six (IL-6), could be controlled through regular consumption of such dietary herbal products without debilitating side effects for their disease-modifying impacts.

Keywords: animal models; cytokines; dietary herbs; neuroinflammation; neurological disorders.

Figure 1

Representative images of Bacopa monnieri, Centella asiatica, Emblica officinalis, Piper nigrum, Mucuna pruriens and Clitoria ternatea, Zingiber officinale, and Punica granatum.

Figure 2

Major bioactive components of Bacopa monnieri (17, 18), Centella asiatica (26), Zingiber officinale (33–35), Punica granatum (43, 44), Emblica officinalis (50, 51), Piper nigrum (54, 55), Mucuna pruriens (58), Clitoria ternatea (65, 66), Moringa oleifera (70), Phoenix dactylifera (82–84) and curcuma longan (90).

Figure 3

Graphical representation of the general effect of herbal dietary products on neuroinflammation and neurological disorders. In conditions of neurological disorders, accumulation of Aβ, tau, α-synuclein, neurofibrillary tangles, plaque formation, neuron degeneration, neurotrauma, or environmental toxicants, or conditions of infections could activate transmembrane pattern-recognition cell surface receptors such as TLRs, particularly in astrocytes and microglia. Activated glial cells secrete IL-1/IL-1β, IL-6, NF-κB, TNF-α, IFN-γ, NO, iNOS, COX-2, CCl2, etc. If unchecked, in conditions such as neurological disorders, chronic inflammation causes enormous functional damage to neurons and glial cells, including astrocytes, microglia, and oligodendrocytes. This could promote the pathogenesis of neurological disorders into an irreversible stage and also could promote systemic inflammation and damage to other organs. When administered, the constituents of the dietary herbs may interfere with these pathways and inhibit the progression of neuroinflammation, thus bringing favorable structural and functional changes in the neurons or preventing additional structural and functional damage to the CNS cells. For example, enriched bioactive components from dietary herbal products could activate pCREB or PI3K/Akt/mTOR pathways or reduce p38, JNK and ERK1/2 pathways and thereby reduce the production of NFκB, TNF-α, IL-1β, iNOS, CCl2, and IL-1, etc. Also, these dietary herbal products may act holistically with various constituents, working synergistically with the healing process using multidimensional mechanisms. This could terminate or slow down the disease propagation.