RETRACTED: Sinomenine inhibits lipopolysaccharide-induced inflammatory injury by regulation of miR-101/MKP-1/JNK pathway in keratinocyte cells

Liu, Shumei; Man, Yigang; Zhao, Li

doi:10.1016/j.biopha.2018.02.086

Cited by 12 publications

(10 citation statements)

References 24 publications

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“…Recent studies start explaining SIN's function through investigating the regulatory effects of SIN on miRNA expression. To data, several miRNAs have been mentioned as downstream genes of SIN, including miR-101 (Liu, Man, & Zhao, 2018), miR-324-5p (Song et al, 2015), and miR-155 (Yu et al, 2013). miR-192 has been mentioned as a differentially expressed miRNA in rheumatoid arthritis synovial tissues, and its expression is associated with fibroblast-like synoviocytes growth (Li, Jin, & Lu, 2017).…”

Section: Gdf11 Was a Target Of Mir-192mentioning

confidence: 99%

Retracted: Lipopolysaccharides‐mediated injury to chondrogenic ATDC5 cells can be relieved by Sinomenine via downregulating microRNA‐192

Wang

Zhang

2019

Phytotherapy Research

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Sinomenine (SIN) is an isoquinoline derived from Caulis Sinomenii that has been used to treat rheumatoid arthritis and osteoarthritis for several decades in China. This study aims to reveal the effects of SIN on mouse chondrogenic ATDC5 cells growth and inflammation. SIN was used to treat ATDC5 cells injured by lipopolysaccharides (LPS). The following parameters were determined for evaluating the treatment effects of SIN: cell viability, apoptosis, reactive oxygen species generation, and pro‐inflammatory cytokines release. Besides, the expression of LPS‐sensitive miRNA (miR‐192) and the activation of NF‐κB and MAPK signaling were studied to explain SIN's function. SIN with concentration of 30 μM significantly attenuated LPS‐induced cell damage via increasing cell viability, inhibiting apoptosis and reactive oxygen species generation, and declining IL‐6 and TNF‐α release. miR‐192 was downregulated by SIN treatment. Restoration of miR‐192 expression by miRNA transfection could significantly impede SIN's protective action. Besides, the inhibitory effects of SIN on the activation of NF‐κB and MAPK signaling were attenuated by miR‐192 overexpression. Furthermore, GDF11 was found to be a target gene of miR‐192. LPS‐mediated injury to chondrogenic ATDC5 cells can be relieved by SIN via downregulating miR‐192 and subsequently repressing the activation of NF‐κB and MAPK signaling.

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Section: Gdf11 Was a Target Of Mir-192mentioning

confidence: 99%

Retracted: Lipopolysaccharides‐mediated injury to chondrogenic ATDC5 cells can be relieved by Sinomenine via downregulating microRNA‐192

Wang

Zhang

2019

Phytotherapy Research

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“…In agreement with our findings, LPS-induced inflammatory injury is reportedly attenuated by down-regulated miR-101 expression and inactivated JNK signalling pathway via the up-regulation of MKP-1 expression. 34 Finally, the anti-inflammatory effect on LPS-activated macrophages could be achieved primarily through the mediation of the miR-101/MKP-1/MAPK axis, with miR-101 as a negative regulator of MKP-1 expression. 15 Additional work is needed to confirm whether miR-101 regulates MKP-1 expression through mRNA degradation or by translational regulation.…”

Section: Discussionmentioning

confidence: 99%

“…33 Furthermore, it was suggested that miR-101 can bind to MKP-1 mRNA 3′UTR and the MAPK/MKP-1/miR-101 axis thus plays a regulatory role in the related immune response and pathogenesis of systemic lupus erythematosus. 34…”

Section: Mir-101 Aggravates Pathological Pain In CCI Rat Models Thrmentioning

confidence: 99%

MiR‐101 promotes pain hypersensitivity in rats with chronic constriction injury via the MKP‐1 mediated MAPK pathway

Qiu

Liu

et al. 2020

J Cellular Molecular Medi

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This study was performed to characterize the effect of microRNA‐101 (miR‐101) on the pain hypersensitivity in CCI rat models with the involvement of mitogen‐activated protein kinase phosphatase 1 (MKP‐1) in spinal cord microglial cells. The mechanical withdrawal threshold (MWT) and thermal withdrawal latency (TWL) in the developed CCI models were determined to assess the hypersensitivity of rats to mechanical stimulation and thermal pain. To assess inflammation, the levels of interleukin (IL)‐1β, IL‐6 and tumour necrosis factor‐α (TNF‐α) in the spinal dorsal horns of CCI rats and lipopolysaccharide (LPS)‐activated microglial cells were examined. miR‐101 and MKP‐1 gain‐ and loss‐of‐function experiments were conducted in in vivo and in vitro settings to examine the roles of miR‐101 and MKP‐1 in CCI hypersensitivity and inflammation. The results showed that miR‐101 was highly expressed in the spinal dorsal horn and microglial cells of CCI rat models. Furthermore, overexpression of miR‐101 promoted the pain hypersensitivity in CCI rat models by reducing MWT and TWL. The overexpression of miR‐101 also promoted inflammation in LPS‐exposed microglial cells, as indicated by increased levels of IL‐1β, IL‐6 and TNF‐α. MiR‐101 was shown to target MKP‐1, inhibiting its expression. Moreover, miR‐101 promoted pain hypersensitivity in CCI rat models by inhibiting MKP‐1 expression and activating the mitogen‐activated protein kinase (MAPK) signalling pathway. Taken together, miR‐101 could potentially promote hypersensitivity and inflammatory response of microglial cells and aggravate neuropathic pain in CCI rat models by inhibiting MKP‐1 in the MAPK signalling pathway.

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“…The immune system is our host defense against various adverse conditions, such as tissue injury from xenobiotic insult [1]. However, over-activated or dysregulated immune responses may conversely result in tissue damage, cellular injury, and molecular dysregulation [2,3]. In spite of the complexity of immune pathogenesis, molecular evidences have indicated that toll-like receptors (TLRs), especially TLR4, play a key role in various in ammatory diseases, such as sepsis, rheumatoid arthritis, asthma, and pneumonia [4][5][6][7].…”

Section: Introductionmentioning

confidence: 99%

The effect of total flavonoids from Saussurea involucrata on the secretion of pro-inflammatory mediators in lipopolysaccharide stimulated RAW264.7 macrophages

Yan

Wang

Cheng

et al. 2020

Preprint

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Background Saussurea involucrate (SI) has long been used to treat inflammatory diseases, such as rheumatoid arthritis. The main active constituents of SI are flavonoids, which are a class of polyphenolic compounds. However, few studies have investigated the anti-inflammatory activity of the total flavonoids of SI (FSI). The mechanism underlying this action is still not fully understood. In the present study, we employed RAW264.7 cell line as an inflammatory cell model to investigate the anti-inflammatory effects of FSI and explore the corresponding molecular mechanisms.Methods We extracted FSI using chromatographic column method. The cell viability was determined by MTT assay. The production of nitric oxide (NO) was detected by Griess assay. The release of cytokines and chemokines were determined by ELISA assays. The nuclear translocation of p65, c-Jun, and IRF3 was detected by immunofluorescence microscopy. Western blotting analysis was performed to determine the related protein expression.Results The results showed that the amount of FSI extracted from SI was 751.5 mg/g. The production of inflammatory mediators was effectively inhibited by FSI. Meanwhile, FSI also suppressed the nuclear translocation of p65, c-Jun, and IRF3. The elevated expression of iNOS, COX-2, p-IKKα/β, p-TBK1, p-IκBα, p-ERK, p-p38, p-JNK, p-p65, p-c-Jun, p-IRF3 induced by LPS was remarkably reduced by FSI treatment.Conclusion These findings indicated that FSI has a potential ability to inhibit the secretion of pro-inflammatory mediators and the underlying mechanism may be related to block the p65, c-Jun, and IRF3 signaling pathways. This study provided evidence for the anti-inflammatory mode and the underlying mechanism of FSI.

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RETRACTED: Sinomenine inhibits lipopolysaccharide-induced inflammatory injury by regulation of miR-101/MKP-1/JNK pathway in keratinocyte cells

Cited by 12 publications

References 24 publications

Retracted: Lipopolysaccharides‐mediated injury to chondrogenic ATDC5 cells can be relieved by Sinomenine via downregulating microRNA‐192

Retracted: Lipopolysaccharides‐mediated injury to chondrogenic ATDC5 cells can be relieved by Sinomenine via downregulating microRNA‐192

MiR‐101 promotes pain hypersensitivity in rats with chronic constriction injury via the MKP‐1 mediated MAPK pathway

The effect of total flavonoids from Saussurea involucrata on the secretion of pro-inflammatory mediators in lipopolysaccharide stimulated RAW264.7 macrophages

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