Anti-Inflammatory Treatments for Chronic Diseases: A Review

Abstract

Inflammation is viewed as one of the major causes for the development of different diseases like cancer, cardiovascular disease, diabetes, obesity, osteoporosis, rheumatoid arthritis, inflammatory bowel disease, asthma, and CNS related diseases such as depression and parkinson's disease; and this fervent phenomenon provides space for understanding different inflammatory markers. Increasing evidences have elucidated the outcome of inflammatory pathways dysregulation resulting in many symptoms of chronic diseases. The detection of transcription factors such as nuclear factor kappa-B (NF-κB), STAT and their gene products such as COX-2, cytokines, chemokines and chemokine receptors has laid molecular foundation for the important role of inflammation in chronic diseases in which the NF-κB is reported as a major mediator which makes a possible way for the development of new therapeutic approaches using synthetic and natural compounds that might eventually decrease the prevalence of these diseases. Even if many inflammatory markers like TNF-α, IL-1, IL-6, IL-8 and C-reactive protein (CRP) are reported to be the major key factors with proved role in several inflammatory diseases, IL-1 and TNF-α are the important cytokines that can induce the expression of NF-κB which is the potential target in these inflammatory diseases. This review aims to explore and summarize that how some drugs and natural compounds show their modulatory activity in inflammatory pathways and chronic inflammatory markers in these inflammatory diseases.

Anti-inflammatory potential of total saponins derived from the roots of Panax ginseng in lipopolysaccharide-activated RAW 264.7 macrophages

“…The inflammatory process is typically highly regulated, consisting of signals that initiate and maintain inflammation, and signals that inhibit the process (4,5). Due to the importance of activated macrophages in the initiation and amplification of a variety of inflammatory diseases, therapeutic methods to reduce the number of activated macrophages, inhibit their activation signals and/or specific macrophage receptors, or to selectively counteract macrophage products, are under investigation for controlling inflammatory diseases (1).…”

“…TNF-α and IL-1β are considered to be critical cytokines in the inflammatory cytokine network, and are produced as a result of endotoxin exposure (2)(3)(4)(5). Furthermore, TNF-α and IL-1β are important for promoting the expression of iNOS, in addition to the production of other cytokines, such as IL-6 and IL-8 (21,25).…”

“…Additionally, excessive inflammatory responses may result in decreased expression of anti-inflammatory cytokines (1,2,4,5). The pathogenesis of autoimmune diseases, which are characterized by chronic inflammation, may be influenced by pro-and anti-inflammatory factors, as well as dysregulation of inflammatory immune responses (5,6).…”

“…The pathogenesis of autoimmune diseases, which are characterized by chronic inflammation, may be influenced by pro-and anti-inflammatory factors, as well as dysregulation of inflammatory immune responses (5,6). Therefore, the utilization of different therapeutic strategies may be therapeutically beneficial for the treatment of inflammatory diseases; for example, bioactive agents could be used to inhibit the production of inflammatory factors by macrophages (4-6).…”

Rap1 GTPase Inhibits Tumor Necrosis Factor-α–Induced Choroidal Endothelial Migration via NADPH Oxidase– and NF-κB–Dependent Activation of Rac1

“…9,10 The roles of TNF-aemediated inflammation in rheumatoid arthritis, Alzheimer disease, atherosclerosis, and diabetes have been well established, 11 and activation of NF-kB by TNF-a plays a fundamental role in these chronic inflammatory diseases. 12 Recent studies also provide evidence to support the role of TNF-a in the regulation of oxidative stress. In microglia cells, TNF-a induced mitochondrial reactive oxygen species (ROS) generation.…”