Curcumin alleviates DSS-induced colitis via inhibiting NLRP3 inflammsome activation and IL-1β production

Gong, Zizhen; Zhao, Shengnan; Zhou, Jun; Yan, Junkai; Wang, Lingyu; Du, Xixi; Li, Hui; Chen, Yingwei; Cai, Wei; Wu, Jin Shang

doi:10.1016/j.molimm.2018.09.004

Cited by 150 publications

(71 citation statements)

References 45 publications

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“…Zhang et al found that the activation of NLRP3/caspase-1 signalling in macrophages can induce bisphosphonate-related osteonecrosis of the jaw in diabetic mice (Zhang et al, 2015). The involvement of NLRP3/ caspase-1 signalling was also found in colitis and neuroinflammation in a mouse model (Fan et al, 2018;Gong et al, 2018).…”

Section: Discussionmentioning

confidence: 99%

NLRP3 inflammasome mediates M1 macrophage polarization and IL‐1β production in inflammatory root resorption

Zhang

Liu

Wan

et al. 2020

J Clinic Periodontology

125

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Aims To explore the involvement of NOD‐like receptor protein 3 (NLRP3) inflammasome and M1 macrophage in root resorption (RR). Methods A rat RR model was established by excessive orthodontic force. After different force‐loading time, the expression levels of NLRP3, caspase‐1, and interleukin‐1β (IL‐1β) and distribution of M1 macrophages were analysed by immunohistochemistry and immunofluorescence staining in vivo. Then, the mechanism of NLRP3 activation was further verified by macrophage and human periodontal ligament cell (hPDLC) co‐culture system in vitro. The production levels of NLRP3, caspase‐1, pro‐caspase‐1, and IL‐1β in M1 macrophages in the co‐culture system were detected by Western blot, and the polarization of CD68+IL‐1β+ M1 macrophages was detected by immunofluorescence staining. Results In the rat RR model, NLRP3, caspase‐1, IL‐1β, and M1 macrophages were expressed in periodontal ligament, mainly concentrated around RR areas. Force‐pre‐treated hPDLCs promoted M1 macrophage polarization and the production of NLRP3, caspase‐1, and IL‐1β in M1 macrophages in co‐culture system. When MCC950, an inhibitor of NLRP3 inflammasome, was added, NLRP3 activation and M1 macrophage polarization were inhibited. Conclusions In periodontal tissues, hPDLCs stimulated by force promoted M1 macrophage polarization and increased IL‐1β production by activating NLRP3 inflammasome in M1 macrophages, thus initiating the occurrence of RR.

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Section: Discussionmentioning

confidence: 99%

NLRP3 inflammasome mediates M1 macrophage polarization and IL‐1β production in inflammatory root resorption

Zhang

Liu

Wan

et al. 2020

J Clinic Periodontology

125

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“…MCC950 has been found to suppress the transcription and translation of IL-1β and IL-18 in both canonical and non-canonical pathways [70]. Curcumin was determined to prevent the key events in the activation step (Signal 2) of the NLRP3 activation pathway; which include K + efflux, ROS formation and cathepsin B release, thus preventing NLRP3 inflammasome activation [71]. Wogonoside was described to inhibit NF-κB activity, which prevents NLRP3 activation in the colon [72].…”

Section: The Nlrp3 Inflammasome and Ibdmentioning

confidence: 99%

Does NLRP3 Inflammasome and Aryl Hydrocarbon Receptor Play an Interlinked Role in Bowel Inflammation and Colitis-Associated Colorectal Cancer?

2020

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Inflammation is a hallmark in many forms of cancer; with colitis-associated colorectal cancer (CAC) being a progressive intestinal inflammation due to inflammatory bowel disease (IBD). While this is an exemplification of the negatives of inflammation, it is just as crucial to have some degree of the inflammatory process to maintain a healthy immune system. A pivotal component in the maintenance of such intestinal homeostasis is the innate immunity component, inflammasomes. Inflammasomes are large, cytosolic protein complexes formed following stimulation of microbial and stress signals that lead to the expression of pro-inflammatory cytokines. The NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been extensively studied in part due to its strong association with colitis and CAC. The aryl hydrocarbon receptor (AhR) has recently been acknowledged for its connection to the immune system aside from its role as an environmental sensor. AhR has been described to play a role in the inhibition of the NLRP3 inflammasome activation pathway. This review will summarise the signalling pathways of both the NLRP3 inflammasome and AhR; as well as new-found links between these two signalling pathways in intestinal immunity and some potential therapeutic agents that have been found to take advantage of this link in the treatment of colitis and CAC.

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“…Curcumin (C 21 H 20 O 6 ) is a natural polyphenolic compound, which can be extracted from the powdered rhizome of the plant Curcuma longa L. Increasing evidence has indicated that curcumin possesses potent antioxidative and anti-inflammatory properties, with minimal side effects in humans (17–19). Notably, the inhibitory effects of curcumin on NLRP3-mediated inflammatory pathways have been reported; for example, Gong et al (20) demonstrated that curcumin effectively improves dextran sulfate sodium (DSS)-induced colitis in mice by inhibiting activation of the NLRP3 inflammasome; this study also reported that inhibiting the NLRP3 inflammasome in vivo with a specific NLRP3 inhibitor notably abrogates the additional inhibitory effects of curcumin on DSS-induced inflammatory bowel disease. Similarly, in fructose-induced hepatic inflammation, curcumin markedly inhibits NLRP3 inflammasome activation by upregulating microRNA-200a in mice, subsequently alleviating hepatic inflammation (21).…”

Section: Introductionmentioning

confidence: 77%

Curcumin relieves paraquat‑induced lung injury through inhibiting the thioredoxin interacting protein/NLR pyrin domain containing 3‑mediated inflammatory pathway

et al. 2019

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When paraquat (PQ) enters the human body, it increases oxidative stress and inflammation, ultimately resulting in acute lung injury (ali). curcumin, a naturally occurring compound, has been reported to ameliorate PQ-induced ali; however, the underlying molecular mechanisms remain unclear. in the present study, normal lung fibroblasts (WI-38VA13) were treated with 10 µmol/l PQ for 48 h, followed by a further 48 h incubation with 300 µmol/l curcumin. cells were then harvested to determine their viability. Flow cytometry was performed to analyze the levels of reactive oxygen species (roS) and the rate of apoptosis. The levels of apoptotic proteins and activation of the thioredoxin interacting protein/NLR pyrin domain containing 3 (TXNIP/NLRP3) axis were measured via reverse transcription-quantitative polymerase chain reaction and western blot analyses. Proinflammatory cytokine levels were examined using enzyme-linked immunosorbent assays. Finally, the expression levels of notch1, extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphorylated-ERK1/2 were evaluated via western blotting. Following treatment with curcumin, PQ-induced increases in roS levels and apoptosis were significantly attenuated, and Bcl-2 expression levels were upregulated, whereas those of Bax were downregulated. It was also observed that curcumin treatment downregulated the expression levels of TXniP, nlrP3, interleukin (il)-1β and IL-18, and downstream caspase-1 compared with PQ treatment alone. Curcumin significantly attenuated the upregulation of Notch1 without affecting ERK1/2 phosphorylation. The present findings suggested that the inhibitory effects of curcumin on TXINP1 may inhibit activation of the NLRP3 inflammasome, subsequently suppressing the upregulation of proinflammatory cytokines and ultimately improving PQ-induced ali.

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Curcumin alleviates DSS-induced colitis via inhibiting NLRP3 inflammsome activation and IL-1β production

Cited by 150 publications

References 45 publications

NLRP3 inflammasome mediates M1 macrophage polarization and IL‐1β production in inflammatory root resorption

NLRP3 inflammasome mediates M1 macrophage polarization and IL‐1β production in inflammatory root resorption

Does NLRP3 Inflammasome and Aryl Hydrocarbon Receptor Play an Interlinked Role in Bowel Inflammation and Colitis-Associated Colorectal Cancer?

Curcumin relieves paraquat‑induced lung injury through inhibiting the thioredoxin interacting protein/NLR pyrin domain containing 3‑mediated inflammatory pathway

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