Abstract
Background: The production and maturation of interleukin (IL)-1β, regulated by the NF-κB and NLRP3 signaling pathways, lie at the core of gout. This study aimed to evaluate the antigout effect of Cichorium intybus L. (also known as chicory) in vivo and in vitro. Methods: A gout animal model was established with monosodium urate (MSU) crystal injections. Rats were orally administered with chicory extract or colchicine. Levels of ankle edema, inflammatory activity, and IL-1β release were observed. Several essential targets of the NF-κB and NLRP3 signaling pathways were detected. Primary macrophages were isolated to verify the antigout mechanism of chicory extract as well as chicoric acid in vitro. Results: Improvements of swelling degree, inflammatory activity, and histopathological lesion in MSU-injected ankles were observed in the treatment with chicory extract. Further, the chicory extract significantly decreased IL-1β release by suppressing the NF-κB and NLRP3 signaling pathways in gout rats. Similar to the in vivo results, IL-1β release was also inhibited by chicory extract and chicoric acid, a specific effective compound in chicory, through the NF-κB and NLRP3 signaling pathways. Conclusion: This study suggests that chicory extract and chicoric acid may be used as promising therapeutic agents against gout by inhibiting the NF-κB and NLRP3 signaling pathways.
Highlights
Gout, characterized by the deposition of monosodium urate (MSU) crystals within intra- and/or periarticular areas, is an inflammatory disease related to excessive circulating uric acid [1]
The first step of nuclear factor kappa-B (NF-κB) activation is required to stimulate the expression of pro-IL-1β [11], and the maturation of IL-1β regulated by the NBD leucine-rich family (NLR) pyrin-containing 3 (NLRP3) inflammasome is the second key step in the initiation of gout flare [12]
To assess the extent of edema, the ankle swelling degree (ASD) of the control and treated rats was calculated by measuring ankle circumference
Summary
Gout, characterized by the deposition of monosodium urate (MSU) crystals within intra- and/or periarticular areas, is an inflammatory disease related to excessive circulating uric acid [1]. Studies suggest that the triggering of interleukin (IL)-1β release, which is activated by MSU stimulation and can further orchestrate a series of inflammatory cascade reactions, lies at the core of gout [10]. Results: Improvements of swelling degree, inflammatory activity, and histopathological lesion in MSU-injected ankles were observed in the treatment with chicory extract. The chicory extract significantly decreased IL-1β release by suppressing the NF-κB and NLRP3 signaling pathways in gout rats. Similar to the in vivo results, IL-1β release was inhibited by chicory extract and chicoric acid, a specific effective compound in chicory, through the NF-κB and NLRP3 signaling pathways. Conclusion: This study suggests that chicory extract and chicoric acid may be used as promising therapeutic agents against gout by inhibiting the NF-κB and NLRP3 signaling pathways
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