Stimulation, regulation, and inflammaging interventions of natural compounds on nuclear factor kappa B (NF-kB) pathway: a comprehensive review.

IF 4.6 2区 医学 Q2 IMMUNOLOGY
Gowtham Kannan, Benedict Mathews Paul, Parimelazhagan Thangaraj
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引用次数: 0

Abstract

Nuclear factor kappa B (NF-kB) is a kind of transcription factor which resides in cytoplasm of each cell and on activation, it translocates to the nucleus. It is activated by a many inducible agents including endotoxins, inflammatory stimuli, carcinogens, pathogens, nicotine, and tumour promoters, etc. NF-kB is activated by canonical and non-canonical signalling pathways which has different signalling compounds and its biological functions. It controls the expression of 400 different genes including various enzymes, cytokines, viral proteins, regulatory molecules involved in the cell cycle etc. This pathway is linked with various ailments including respiratory diseases, inflammatory diseases, auto immune diseases, cancer and diabetes. NF-kB factor and signalling pathway are the mainstream of the innate and adaptive immune responses. Human subjects have been able to curb inflammation through inflammaging with the help of the phytomolecules interacting with the NF-κB pathway by adjusting the inflammation processes and alleviating aging stresses in cells. They successfully inhibit the activation of NF-κB, thereby curtailing chronic low-grade inflammation underlying both ageing and age-related disease processes. These phytocompounds discussed herewith not only down-regulate NF-κB-dependent pro-inflammatory pathways but also help build resilience at cellular levels, therefore, offering enhanced healthspan with late commencement of inflammaging pathogenesis. This review describes what stimulation and regulation of the Nuclear Factor kappa B (NF-kB) Pathway and its roles in the pathogenesis of human age related diseases. We also review the recent progress in attenuating the molecular mechanisms of the NF-kB Pathway by phytochemicals, which may open up novel therapeutic avenues.

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来源期刊
Inflammopharmacology
Inflammopharmacology IMMUNOLOGYTOXICOLOGY-TOXICOLOGY
CiteScore
8.00
自引率
3.40%
发文量
200
期刊介绍: Inflammopharmacology is the official publication of the Gastrointestinal Section of the International Union of Basic and Clinical Pharmacology (IUPHAR) and the Hungarian Experimental and Clinical Pharmacology Society (HECPS). Inflammopharmacology publishes papers on all aspects of inflammation and its pharmacological control emphasizing comparisons of (a) different inflammatory states, and (b) the actions, therapeutic efficacy and safety of drugs employed in the treatment of inflammatory conditions. The comparative aspects of the types of inflammatory conditions include gastrointestinal disease (e.g. ulcerative colitis, Crohn''s disease), parasitic diseases, toxicological manifestations of the effects of drugs and environmental agents, arthritic conditions, and inflammatory effects of injury or aging on skeletal muscle. The journal has seven main interest areas: -Drug-Disease Interactions - Conditional Pharmacology - i.e. where the condition (disease or stress state) influences the therapeutic response and side (adverse) effects from anti-inflammatory drugs. Mechanisms of drug-disease and drug disease interactions and the role of different stress states -Rheumatology - particular emphasis on methods of measurement of clinical response effects of new agents, adverse effects from anti-rheumatic drugs -Gastroenterology - with particular emphasis on animal and human models, mechanisms of mucosal inflammation and ulceration and effects of novel and established anti-ulcer, anti-inflammatory agents, or antiparasitic agents -Neuro-Inflammation and Pain - model systems, pharmacology of new analgesic agents and mechanisms of neuro-inflammation and pain -Novel drugs, natural products and nutraceuticals - and their effects on inflammatory processes, especially where there are indications of novel modes action compared with conventional drugs e.g. NSAIDs -Muscle-immune interactions during inflammation [...]
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