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Inflammation is a necessary functional response triggered by invading pathogens or damaged tissue. It helps isolate an injured area or foreign substance from further contact with body tissue and triggers phagocytes to remove pathogens, injured tissue and dead cells. However, when inflammation persists, it may give rise to further tissue damage potentially leading to serious disorders due to the excessive production of inflammatory cytokines. IL-1Beta is a proinflammatory cytokine that influences several levels of immune responses, physiological processes and participates in pain development. Many chronic inflammatory diseases are related to the overproduction of IL-1Beta.
NLRP3 Inflammasome is a multiprotein complex that triggers the release of IL-1Beta. NLRP3 requires two levels of activation. The first signal induces the expression of NLRP3 and pro- IL-1Beta and the second signal activates the complex. The primary function of this process is to protect the host. However, exogenous and endogenous non-microbial compounds also effectively induce activation of NLRP3 inflammasome leading to sterile inflammation, allergic responses or other forms of inflammation.
This article provides an overview of studies that demonstrated the effect of plant-derived natural compounds on NLRP3 inflammasome-mediated IL-1Beta. The authors chose to focus on natural compounds that have been in long-term use in traditional medicine. These compounds are considered complementary supplements used in the support of healthy inflammatory pathways, making them good candidates to study NLRP3 function. Resveratrol and Quercetin were highlighted.
Radiation-induced increase in IL-1β occurs via the NLRP3 inflammasome activation; however, resveratrol attenuated the expression of NLRP3. It was also demonstrated that resveratrol treatment upregulated the expression of Sirt1. In conclusion, it is suggested that Sirt1 inhibits NFκB transcriptional activity through deacetylation that in turn limits the transcription of NLRP3.
...it was shown that quercetin markedly inhibited the overexpression of hepatic TXNIP, in addition to reducing the production of ROS and the activation of NLRP3 inflammasome, consequently resulting in decreased IL-1β secretion.
The authors concluded that clarification of the molecular mechanism of action of such natural compounds, already used in traditional medicine for quite some time, will undoubtedly support healthy inflammatory pathways in the event of NLRP3 inflammasome-mediated IL-1β overproduction.
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