Curcumin analogue AI-44 alleviates MSU-induced gouty arthritis in mice via inhibiting cathepsin B-mediated NLRP3 inflammasome activation

Gu, Yanpin; Zhu, Yong; Deng, Guoliang; Liu, Songjun; Sun, Yang; Lv, Wen

doi:10.1016/j.intimp.2021.107375

Cited by 21 publications

(16 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This can be attributed to the usage of Ficoll density gradient centrifugation to extract PBMCs, which did not contain neutrophils. What's more, gouty arthritis is attributed to acute inflammation characterized by the recruitment of macrophages and MSU crystal deposition-induced neutrophils in the joints ( 34 ). In our study, we isolated and treated neutrophils with MSU to establish an in vitro model, while MSU crystals were injected to construct a mouse model of acute gouty arthritis.…”

Section: Discussionmentioning

confidence: 99%

RETRACTED: NFIL3 Facilitates Neutrophil Autophagy, Neutrophil Extracellular Trap Formation and Inflammation During Gout via REDD1-Dependent mTOR Inactivation

et al. 2021

View full text Add to dashboard Cite

Autophagy pathways play an important role in immunity and inflammation via pathogen clearance mechanisms mediated by immune cells, such as macrophages and neutrophils. In particular, autophagic activity is essential for the release of neutrophil extracellular traps (NETs), a distinct form of active neutrophil death. The current study set out to elucidate the mechanism of the NFIL3/REDD1/mTOR axis in neutrophil autophagy and NET formation during gout inflammation. Firstly, NFIL3 expression patterns were determined in the peripheral blood neutrophils of gout patients and monosodium urate (MSU)-treated neutrophils. Interactions between NFIL3 and REDD1 were identified. In addition, gain- or loss-of-function approaches were used to manipulate NFIL3 and REDD1 in both MSU-induced neutrophils and mice. The mechanism of NFIL3 in inflammation during gout was evaluated both in vivo and in vitro via measurement of cell autophagy, NET formation, MPO activity as well as levels of inflammatory factors. NFIL3 was highly-expressed in both peripheral blood neutrophils from gout patients and MSU-treated neutrophils. NFIL3 promoted the transcription of REDD1 by binding to its promoter. REDD1 augmented neutrophil autophagy and NET formation by inhibiting the mTOR pathway. In vivo experimental results further confirmed that silencing of NFIL3 reduced the inflammatory injury of acute gouty arthritis mice by inhibiting the neutrophil autophagy and NET formation, which was associated with down-regulation of REDD1 and activation of the mTOR pathway. Taken together, NFIL3 can aggravate the inflammatory reaction of gout by stimulating neutrophil autophagy and NET formation via REDD1/mTOR, highlighting NFIL3 as a potential therapeutic target for gout.

show abstract

Section: Discussionmentioning

confidence: 99%

RETRACTED: NFIL3 Facilitates Neutrophil Autophagy, Neutrophil Extracellular Trap Formation and Inflammation During Gout via REDD1-Dependent mTOR Inactivation

et al. 2021

View full text Add to dashboard Cite

show abstract

“…153 Now, mono-carbonyl derivatives are a major direction in the structural modification of curcumin. In the structural design of mono-carbonyl curcumin derivatives, ketenone 154 is commonly used to replace β-dione, and can also be combined with cyclopentanone, cyclohexanone, 155,156 4-piperidone 157 or N-substituted −4-piperidone. 158,159 At the same time, the "ortho effect" of the ortho substituents on the benzene ring is emphasized and utilized.…”

Section: Derivatives and Prodrugs Of Curcuminmentioning

confidence: 99%

Anti-Inflammatory Effects of Curcumin in the Inflammatory Diseases: Status, Limitations and Countermeasures

Peng¹,

Ao²,

BaoHua³

et al. 2021

DDDT

294

157

View full text Add to dashboard Cite

“…Gout is a well-known P2X7/caspase-1-related disease elicited by the deposition of MSU with a typical first presentation of intensely painful acute inflammatory arthritis, and MSU-promoted macrophage recruitment as well as downstream pyroptosis contribute to inflammatory pain. 10,61,62 The current therapeutic strategy for gout includes the application of colchicine and IL-1β inhibitor. Unfortunately, limitations such as adverse reactions, sensitivity difference, financial burden and inconvenient administration routes make it urgent to explore novel small-molecule caspase-1 inhibitors.…”

Section: Papermentioning

confidence: 99%

Sennoside A is a novel inhibitor targeting caspase-1

Lan

Shi

et al. 2022

Food Funct.

View full text Add to dashboard Cite

show abstract

Curcumin analogue AI-44 alleviates MSU-induced gouty arthritis in mice via inhibiting cathepsin B-mediated NLRP3 inflammasome activation

Cited by 21 publications

References 29 publications

RETRACTED: NFIL3 Facilitates Neutrophil Autophagy, Neutrophil Extracellular Trap Formation and Inflammation During Gout via REDD1-Dependent mTOR Inactivation

RETRACTED: NFIL3 Facilitates Neutrophil Autophagy, Neutrophil Extracellular Trap Formation and Inflammation During Gout via REDD1-Dependent mTOR Inactivation

Anti-Inflammatory Effects of Curcumin in the Inflammatory Diseases: Status, Limitations and Countermeasures

Sennoside A is a novel inhibitor targeting caspase-1

Contact Info

Product

Resources

About