Sinomenine Attenuates Cartilage Degeneration by Regulating miR-223-3p/NLRP3 Inflammasome Signaling

Haichao, Dong; Li, Peinan; Chen, Chang-Jian; Xu, Xin; Zhang, Hong; Liu, Gang; Lianjie, Zheng; Li, Peng

doi:10.1007/s10753-019-00986-3

Cited by 50 publications

(40 citation statements)

References 40 publications

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“…Recently, several reports have confirmed that miR‐223 directly targets NLRP3 32‐34 . Our results also confirmed that miR‐223‐3p negatively regulates the NLRP3 expression, by using a dual‐luciferase assay, and also that this process occurs in syphilis patients and HUVECs stimulated with rTP17.…”

Section: Discussionsupporting

confidence: 86%

“…Recently, several reports have confirmed that miR-223 directly targets NLRP3. [32][33][34] Our results also confirmed that miR-223-3p negatively regulates the NLRP3 expression, by using a dual-luciferase assay, and also that this process occurs in syphilis patients and HUVECs stimulated with rTP17. Moreover, we found that NLRP3 overexpression could block the inhibitory effects of miR-223-3p on inflammasome activation and pyroptosis in the HUVECs stimulated with rTP17.…”

Section: Discussionsupporting

confidence: 82%

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MiR‐223‐3p inhibits rTp17‐induced inflammasome activation and pyroptosis by targeting NLRP3

Long

Kou

et al. 2020

J Cellular Molecular Medi

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Section: Discussionsupporting

confidence: 86%

Section: Discussionsupporting

confidence: 82%

MiR‐223‐3p inhibits rTp17‐induced inflammasome activation and pyroptosis by targeting NLRP3

Long

Kou

et al. 2020

J Cellular Molecular Medi

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“…Our previous research showed that miR-223-3p might be a key miRNA in the relief of neuralgia by EA [23]. miR-223-3p was reported to suppress the activity of inflammasomes and was involved in regulating inflammation [34,35]. Under physiological conditions, pain signals are transmitted from the peripheral nerve to the spinal cord via Aδ and C fibers.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture Inhibits Autophagy of Neuron Cells in Postherpetic Neuralgia by Increasing the Expression of miR-223-3p

Zou

Dong

Wang

et al. 2021

BioMed Research International

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Postherpetic neuralgia (PHN) is a complication of herpes zoster viral infection. Its main manifestations are continuous or intermittent burning-like and electroshock-like pain in the affected nerves. Electroacupuncture (EA) is widely used in clinical treatment and exerts effects in alleviating neuropathic pain. In this study, we investigated the effect and underlying mechanism of EA on PHN. Sprague-Dawley rats were treated with resiniferatoxin (RTX) to establish a PHN model and subjected to EA and/or miR-223-3p overexpression (OV) or interference. Mechanical withdrawal latency was measured as an indication of pain sensitivity. Hematoxylin-eosin staining and transmission electron microscopy were performed to observe glial cell morphology and autophagic vacuoles, respectively. ELISA was performed to detect reactive oxygen species (ROS) production and the levels of tumor necrosis factor- (TNF-) α, inducible nitric oxide synthase (iNOS), interleukin- (IL-) 6, and IL-10. Changes in autophagy and apoptosis-related miRNAs were detected by immunofluorescence and qRT-PCR, respectively. In RTX-treated rats, OV and EA reduced pain sensitivity, decreased the number of eosinophils, and increased that of nerve cells. ROS generation and the levels of TNF-α and iNOS were significantly reduced, while those of IL-6 and IL-10 were increased. OV and EA induced fewer autophagic vacuoles than those in the model group. The expression of autophagy-related protein microtubule-associated protein 1 light chain 3-II, ATG9, and Rab1 was decreased by OV and EA, whereas that of P62 was increased. qRT-PCR revealed that miR-223-3p expression in the model group decreased but was increased by EA. EA inhibits glial cell autophagy in PHN by increasing miR-223-3p expression.

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“…25 In the process of pyroptosis, cleave caspase-1 could trigger the maturation and secretion of IL-1β and IL-18 and then expand inflammatory reaction. 26 And the inhibition of caspase-1 could slow down the development of chronic arthritis. 27 IL-1β, as one of the most prominent inflammation cytokines in OA, has been considered to be implicated in cartilage degradation.…”

Section: F I G U R Ementioning

confidence: 99%

Activating Nrf2 signalling alleviates osteoarthritis development by inhibiting inflammasome activation

Yan

Zhan

et al. 2020

J Cellular Molecular Medi

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Osteoarthritis (OA), which is characterized by proliferation of subchondral bone and the degeneration of articular cartilage, is the most prevalent human arthritis. Nod‐like receptor pyrin domain 3 (NLRP3) inflammasome is a hot spot in recent year and has been reported to be associated with OA synovial inflammation. However, there are few studies on NLRP3 inflammasome in chondrocyte. Licochalcone A (Lico A), a compound extracted from Glycyrrhiza species, has various biological effects such as anti‐inflammation, anti‐apoptotic, anti‐cancer and anti‐oxidation. In this study, we investigated the protective effect of Lico A on chondrocytes stimulated by lipopolysaccharide (LPS) and surgically induced OA models. In vitro, Lico A could reduce the expression of NLRP3, apoptosis‐associated speck‐like protein (ASC), Gasdermin D (GSDMD), caspase‐1, interleukin‐1beta (IL‐1β) and IL‐18, which indicated that Lico A attenuates LPS‐induced chondrocytes pyroptosis. In addition, Lico A ameliorates the degradation of extracellular matrix (ECM) by enhancing the expression of aggrecan and collagen‐II. Meanwhile, we found that Lico A inhibits NLRP3 inflammasome via nuclear factor erythroid‐2‐related factor 2 (Nrf2)/haeme oxygenase‐1(HO‐1)/nuclear factor kappa‐B (NF‐κB) axis. And the Nrf2 small interfering RNA (siRNA) could reverse the anti‐pyroptosis effects of Lico A in mouse OA chondrocytes. In vivo, Lico A mitigates progression OA in a mouse model and reduces OA Research Society International (OARSI) scores. Thus, Lico A may have therapeutic potential in OA.

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Sinomenine Attenuates Cartilage Degeneration by Regulating miR-223-3p/NLRP3 Inflammasome Signaling

Cited by 50 publications

References 40 publications

MiR‐223‐3p inhibits rTp17‐induced inflammasome activation and pyroptosis by targeting NLRP3

MiR‐223‐3p inhibits rTp17‐induced inflammasome activation and pyroptosis by targeting NLRP3

Electroacupuncture Inhibits Autophagy of Neuron Cells in Postherpetic Neuralgia by Increasing the Expression of miR-223-3p

Activating Nrf2 signalling alleviates osteoarthritis development by inhibiting inflammasome activation

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