Caffeic Acid Phenethyl Ester Prevents Colitis-Associated Cancer by Inhibiting NLRP3 Inflammasome

Dai, Guoliang; Jiang, Zhitao; Sun, Baoyun; Liu, Chao; Meng, Qingcai; Ding, Kang; Wen, Jing; Ju, Wenzheng

doi:10.3389/fonc.2020.00721

Cited by 38 publications

(22 citation statements)

References 35 publications

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“…The effects appear to be by inhibition of ROS release and NLRP3. [194][195][196][197][198] Several other molecules inhibiting caspase-1, IL-1β, GSDMD, PAMP, and DAMP have also been proposed for regulating inflammasome activation in immune-mediated disorders. L-sulforaphane, a phytochemical derived from broccoli and a potential caspase-1 inhibitor is currently in clinical trials for several immune-mediated disorders like asthma, allergy, and rhinitis.…”

Section: Inflammasome Inhibitory Molecules As a Therapeutic Approach In Ibdmentioning

confidence: 99%

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Therapeutic implications of inflammasome in inflammatory bowel disease

Khatri

Kalyanasundaram

2021

FASEB j.

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Inflammatory bowel disease (IBD) remains a persistent health problem with a global burden surging over 6.8 million cases currently. Clinical pathology of IBD is complicated; however, hyperactive inflammatory and immune responses in the gut is shown to be one of the persistent causes of the disease. Human gut inflammasome, the activator of innate immune system is believed to be a primary underlying cause for the pathology and is largely associated with the progression of IBD. To manage IBD, there is a need to fully understand the role of inflammasome activation in IBD.Since inflammasome potentially play a significant role in IBD, systemic modulation of inflammasome may provide an effective therapeutic and clinical approach to control IBD symptoms. In this review, we have focused on this association between IBD and gut inflammasome, and recent advances in the research and therapeutic strategies for IBD. We have discussed inflammasomes and their components, outcomes from the experimental animals and human studies, inflammasome inhibitors, and developments in the inflammasome-targeted therapies for IBD.

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Section: Inflammasome Inhibitory Molecules As a Therapeutic Approach In Ibdmentioning

confidence: 99%

“…Similarly, flavonoid VI‐16, plumercin, procyanidin, dimethyl fumarate, and caffeic acid phenethyl ester are found to be therapeutically effective in ameliorating experimental mouse models of colitis. The effects appear to be by inhibition of ROS release and NLRP3 194‐198 …”

Section: Inflammasome Inhibitory Molecules As a Therapeutic Approach In Ibdmentioning

confidence: 99%

Therapeutic implications of inflammasome in inflammatory bowel disease

Khatri

Kalyanasundaram

2021

FASEB j.

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“…A recent study [ 91 ] showed that CAPE suppressed caspase-1 autocleavage, IL-1β release, and inflammasome formation in both THP-1 cells and BMDMs when the NLRP3 inflammasome was activated using LPS and ATP. The level of NLRP3 protein was decreased in a dose-dependent manner by CAPE treatment.…”

Section: Recently Identified Natural Compounds With Anti-nlrp3 Infmentioning

confidence: 99%

Anti-NLRP3 Inflammasome Natural Compounds: An Update

Liu

2021

Biomedicines

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The nucleotide-binding domain and leucine-rich repeat related (NLR) family, pyrin domain containing 3 (NLRP3) inflammasome is a multimeric protein complex that recognizes various danger or stress signals from pathogens, the host, and the environment, leading to activation of caspase-1 and inducing inflammatory responses. This pro-inflammatory protein complex plays critical roles in pathogenesis of a wide range of diseases including neurodegenerative diseases, autoinflammatory diseases, and metabolic disorders. Therefore, intensive efforts have been devoted to understanding its activation mechanisms and to searching for its specific inhibitors. Approximately forty natural compounds with anti-NLRP3 inflammasome properties have been identified. Here, we provide an update about new natural compounds that have been identified within the last three years to inhibit the NLRP3 inflammasome and offer an overview of the underlying molecular mechanisms of their anti-NLRP3 inflammasome activities.

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“…Colonic villi were abundant in the atractylenolide I group, and the height was significantly increased (Figure 4A). The NLRP3 inflammasomes have been shown to play a key role in AOM/DSS-induced caCRC model (Dai et al, 2020). To determine whether atractylenolide I inhibits NLRP3 inflammasomes in vivo, we evaluated the expression of NLRP3 in the AOM/DSS mice model by immunohistochemistry (IHC) and Western blotting.…”

Section: Atractylenolide I Inhibited Nlrp3 Inflammasome Formation and Activationmentioning

confidence: 99%

Atractylenolide I Inhibits NLRP3 Inflammasome Activation in Colitis-Associated Colorectal Cancer via Suppressing Drp1-Mediated Mitochondrial Fission

Yao

Yang

et al. 2021

Front. Pharmacol.

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Inflammatory bowel disease (IBD) is an important high-risk factor that promotes the occurrence and development of colon cancer. Research on the mechanism of regulating NLRP3 can provide potential targets for treating NLRP3 inflammasome–related diseases and changing the inflammatory potential of immune cells. In this study, the effects of atractylenolide I on colitis-associated CRC (caCRC) and inflammasome activation were investigated both in vivo and in vitro. Furthermore, the role of atractylenolide I on Drp1-mediated mitochondrial fission was analyzed via Western blotting and transmission electron microscopy (TEM). Moreover, the Drp1 overexpression lentiviral vector was used to study the role of Drp1 on the signaling mechanisms of atractylenolide I. Atractylenolide I treatment significantly reduced the cell viability of human HCT116 and SW480 cells and induced apoptosis, and effectively inhibited colon tumors in the AOM/DSS mouse model. The reduction of NLRP3 inflammasome activation and excessive fission of mitochondria mediated by Drp1 were associated with the administration of atractylenolide I. Upregulation of Drp1 reversed the inhibitory effect of atractylenolide I on the activation of NLRP3 inflammasomes. Overexpressing the Drp1 expression counteracted the restraint of atractylenolide I on the release of IL-1β of LPS/DSS-stimulated BMDMs. Atractylenolide I inhibited NLRP3 and caspase-1 expression in mice BMDMs, with no influence in the Drp1-overexpressed BMDMs. These results demonstrated that atractylenolide I inhibits NLRP3 inflammasome activation in colitis-associated colorectal cancer via suppressing Drp1-mediated mitochondrial fission.

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Caffeic Acid Phenethyl Ester Prevents Colitis-Associated Cancer by Inhibiting NLRP3 Inflammasome

Cited by 38 publications

References 35 publications

Therapeutic implications of inflammasome in inflammatory bowel disease

Therapeutic implications of inflammasome in inflammatory bowel disease

Anti-NLRP3 Inflammasome Natural Compounds: An Update

Atractylenolide I Inhibits NLRP3 Inflammasome Activation in Colitis-Associated Colorectal Cancer via Suppressing Drp1-Mediated Mitochondrial Fission

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