Tamarixinin A Alleviates Joint Destruction of Rheumatoid Arthritis by Blockade of MAPK and NF-κB Activation

Zhuang, Yuanyuan; Liu, Jiabao; Ma, Pei; Bai, Jinye; Ding, Yasi; Yang, Hui; Fan, Yannan; Lin, Mingbao; Li, Shuai; Hou, Qi

doi:10.3389/fphar.2017.00538

Cited by 20 publications

(10 citation statements)

References 29 publications

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“…[29][30][31][32] LPS increases the secretion of pro-inflammatory cytokines in fibroblast-like synoviocytes, which leads to the activation of the PI3K/ AKT and MAPK/mTOR pathways, thereby inducing apoptotic and inflammatory injury in these cells. [29][30][31][32] LPS increases the secretion of pro-inflammatory cytokines in fibroblast-like synoviocytes, which leads to the activation of the PI3K/ AKT and MAPK/mTOR pathways, thereby inducing apoptotic and inflammatory injury in these cells.…”

Section: Discussionmentioning

confidence: 99%

Retracted: miR‐145 eliminates lipopolysaccharides‐induced inflammatory injury in human fibroblast‐like synoviocyte MH7A cells

Zhong

Yang

et al. 2018

J of Cellular Biochemistry

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Recently, it has been accepted that miR-based therapy may be beneficial for rheumatoid arthritis (RA). This study aimed to evaluate the potential involvement of miR-145 in RA in vitro. The expression of miR-145 in the human fibroblast-like synoviocyte line MH7A was overexpressed by miR-mimic transfection, after which cells were subjected to lipopolysaccharides (LPS). Cell viability, apoptosis, and the release of pro-inflammatory cytokines were measured. The result showed that the apoptosis and the release of IL-1β, IL-6, IL-8, and TNF-α were significantly induced by LPS. Meanwhile, LPS treatment led to downregulation of miR-145. miR-145 overexpression in LPS-untreated MH7A cells had no impacts on cell apoptosis and inflammation. But, restoring miR-145 expression in LPS-stimulated cells by supplementation of a miR-145 mimic protected MH7A cells against LPS-induced apoptosis and inflammation. Furthermore, miR-145 overexpression in LPS-untreated MH7A cells slightly blocked the PI3K/ATK and mTOR pathways, whereas miR-145 overexpression in LPS-stimulated cells notably repressed the LPS-induced activation of PI3K/ATK and MAPK/mTOR pathways. Our study suggested that miR-145 protected MH7A cells against LPS-induced apoptosis and inflammation by inhibiting the PI3K/AKT and MAPK/mTOR pathways.

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Section: Discussionmentioning

confidence: 99%

Retracted: miR‐145 eliminates lipopolysaccharides‐induced inflammatory injury in human fibroblast‐like synoviocyte MH7A cells

Zhong

Yang

et al. 2018

J of Cellular Biochemistry

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“…Previous studies indicated that synovial inflammatory cells were significantly decreased after the anti-TNF-α mAb treatment, suggesting that TNFα played an important role in RA pathogenesis [37][38][39]. e key pathogenesis of RA was overexpressed inflammatory cytokines and tissue injury mediated by persistent NFkappa B activation, and agents could alleviate RA phenotype by blockade of NF-kappa B activation [40,41]. Recent work indicated that the insufficient apoptosis of inflammatory cells in the RA joint might contribute to pathogenesis, and induction of inflammatory cells apoptosis is a feasible strategy for treating RA [42].…”

Section: Discussionmentioning

confidence: 99%

Deciphering the Active Ingredients and Molecular Mechanisms of Tripterygium hypoglaucum (Levl.) Hutch against Rheumatoid Arthritis Based on Network Pharmacology

Jiang

Zhong

Long

et al. 2020

Evidence-Based Complementary and Alternative Medicine

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Tripterygium hypoglaucum (Levl.) Hutch (THH) shows well clinical effect on rheumatoid arthritis (RA), but the active ingredients and molecular mechanisms remain unclear. This work was designed to explore these issues by network pharmacology. Compounds from THH were gathered by retrieving literatures. Compound-related and RA-related genes were identified using databases, and the overlapping genes were identified by Venn diagram. The active ingredients and genes of THH against RA were confirmed by dissecting interactions between overlapping genes and compounds using Cytoscape. SystemsDock website was used to further verify the combining degree of key genes with active ingredients. Pathway enrichment analysis was performed to decipher the mechanisms of THH against RA by Database for Annotation, Visualization and Integrated Discovery. A total of 123 compounds were collected, and 110 compounds-related and 1871 RA-related genes were identified, including 64 overlapping genes. The target genes and active ingredients of THH against RA comprised 64 genes and 17 compounds, the focus of which was PTGS2, triptolide, and celastrol. SystemsDock website indicated that the combing degree of PTGS2 with triptolide or celastrol was very good. The mechanisms of THH against RA were linked to 31 signaling pathways, and the key mechanism was related to inhibition of inflammation response through inactivating TNF and NF-kappa B signaling pathways. This work firstly explored the active ingredients and mechanisms of THH against RA by network pharmacology and provided evidence to support clinical effects of THH on RA.

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“…Fibroblast-like synoviocytes (FLSs), which can be cancerous and can destroy cartilage, participate in synovitis, are the main effectors of bone destruction in RA. The raised invasiveness of these cells is closely related to the pathogenesis and progression of RA (Zhuang et al 2017). Numerous studies have shown that FLSs in RA patients can abnormally produce high levels of matrix metalloproteinases (MMPs), which are important effector molecules of bone destruction (Huang et al 2017).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-21-5p are involved in apoptosis and invasion of fibroblast-like synoviocytes through PTEN/PI3K/AKT signal

et al. 2019

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The function of microRNA-21-5p (miR-21) in fibroblast-like synoviocytes in RA was still unclear. In our study, we used tumor necrosis factor alpha (TNFa) (10 ng/ml) to mimic RA-FLSs and we found that normal FLS stimulated with TNFa caused the increasing expression of miR-21, a disintegrin and metalloproteinase with thrombospondin motifs 5 and matrix metalloproteinase 3, which were in accord with RA-FLSs changes. Our data showed that miR-21 overexpression significantly increased cell invasion and decreased apoptosis in FLSs. Knockdown of miR-21 in FLSs causes the opposite result. However, miR-21 may not affect the proliferation of FLSs. Meanwhile, we showed that miR-21 activated the PI3K/ AKT signaling pathway to participate in RA by inhibiting PTEN expression. Taken together, our results suggested that miR-21 may play a positive role in RA and may be a promising new therapeutic target for RA. Keywords Fibroblast-like synoviocytes Á MicroRNA-21-5p Á Apoptosis Á Invasion Á PTEN/PI3K/ AKT signal Xin Yan and Yake Liu have contributed equally to this work.

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Tamarixinin A Alleviates Joint Destruction of Rheumatoid Arthritis by Blockade of MAPK and NF-κB Activation

Cited by 20 publications

References 29 publications

Retracted: miR‐145 eliminates lipopolysaccharides‐induced inflammatory injury in human fibroblast‐like synoviocyte MH7A cells

Retracted: miR‐145 eliminates lipopolysaccharides‐induced inflammatory injury in human fibroblast‐like synoviocyte MH7A cells

Deciphering the Active Ingredients and Molecular Mechanisms of Tripterygium hypoglaucum (Levl.) Hutch against Rheumatoid Arthritis Based on Network Pharmacology

MicroRNA-21-5p are involved in apoptosis and invasion of fibroblast-like synoviocytes through PTEN/PI3K/AKT signal

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