Neuroinflammation Mechanisms and Phytotherapeutic Intervention: A Systematic Review

Abstract

Neuroinflammation is indicated in the pathogenesis of several acute and chronic neurological disorders. Acute lesions in the brain parenchyma induce intense and highly complex neuroinflammatory reactions with similar mechanisms among various disease prototypes. Microglial cells in the CNS sense tissue damage and initiate inflammatory responses. The cellular and humoral constituents of the neuroinflammatory reaction to brain injury contribute significantly to secondary brain damage and neurodegeneration. Inflammatory cascades such as proinflammatory cytokines from invading leukocytes and direct cell-mediated cytotoxicity between lymphocytes and neurons are known to cause "collateral damage" in models of acute brain injury. In addition to degeneration and neuronal cell loss, there are secondary inflammatory mechanisms that modulate neuronal activity and affect neuroinflammation which can even be detected at the behavioral level. Hence, several of health conditions result from these pathogenetic conditions which are underlined by progressive neuronal function loss due to chronic inflammation and oxidative stress. In the first part of this Review, we discuss critical neuroinflammatory mediators and their pathways in detail. In the second part, we review the phytochemicals which are considered as potential therapeutic molecules for treating neurodegenerative diseases with an inflammatory component.

Neurogenic Appendicitis: A Reappraisal of the Clinicopathological Features and Pathogenesis

“…Neuroinflammation is a tissue response mediated by the neural cells, NPs, and yet unidentified mediators. It is involved in the development of NA [ 29 , 72 , 73 ] by inducing the hyperplasia of the neuroendocrine cells and the proliferation of the nerve fibers. These lead to an enhanced release of NPs in the wall of the appendix.…”

Molecular Mechanisms and Therapeutic Potential of α- and β-Asarone in the Treatment of Neurological Disorders

“…Plant-derived secondary metabolites with strong antioxidant capacities can reduce the prevalence of age-related neurological disorders associated with increased inflammation [ 146 , 147 ]. In vitro and in vivo experiments have shown that, by attenuating the expression of pro-inflammatory cytokines and inflammatory mediators, including tumour necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1β, preventing inflammasome formation, or inducing the expression of neuroprotective anti-inflammatory and antioxidant molecules, α- and β-asarone can exert neuroprotective effects in various neurological disorders [ 78 , 82 ] ( Figure 2 ).…”

Beneficial Impacts of Alpha-Eleostearic Acid from Wild Bitter Melon and Curcumin on Promotion of CDGSH Iron-Sulfur Domain 2: Therapeutic Roles in CNS Injuries and Diseases

“…Primary trauma leads to structural destruction of vital organs, including cell membrane disruption, myelin and axon destruction, as well as neurovascular injury, which further triggers secondary injuries [29]. Specifically, the activation of astrocytes and microglia in the neuroinflammation process involves a complex mechanism of secondary damage to the CNS [30,31]. In a mouse model of TBI, damage-triggered changes in astrocyte morphology have been shown to be accompanied by alternative localization and aggregation of γ-synuclein, indicating potential neurodegenerative changes following CNS injuries [32].…”