Sinapic Acid Inhibits the IL-1β-Induced Inflammation via MAPK Downregulation in Rat Chondrocytes

Huang, Xiaojian; Pan, Quan-Ke; Mao, Zekai; Zhang, Rui; Ma, Xiaohu; Xi, Yong; You, Hongbo

doi:10.1007/s10753-017-0712-4

Cited by 33 publications

(26 citation statements)

References 26 publications

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“…Cox-2 mainly exists in the nuclear membrane and is not expressed in resting state only when chondrocytes were stimulated by IL-1b and other substances. Previous studies have found that controlling the expression of Cox-2 could suppress the inflammation in the early stage of OA, so as to alleviate symptoms and relieve pain [21]. We also found that IL-1b induced overexpression of Cox-2 and the combination with LBP suppressed the level of Cox-2.…”

Section: Discussionsupporting

confidence: 61%

RETRACTED ARTICLE: Lycium barbarum polysaccharide alleviates IL-1β-evoked chondrogenic ATDC5 cell inflammatory injury through mediation of microRNA-124

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Background: Lycium barbarum polysaccharide (LBP) is a promising therapeutic drug in inflammationrelated injuries, nevertheless the mechanism of LBP's action is still elusive. The study is to explore the effect of LBP on IL-1b-evoked ATDC5 cell inflammatory injury. Methods: ATDC5 cells were administrated with 10 ng/mL interleukin (IL)-1b to establish an in vitro model of cartilage damage. After management, cell viability was tested through CCK8 assay. The proinflammatory cytokines and cyclooxygenase (Cox)-2 were assessed through ELISA, western blot and qRT-PCR. MiR-124 expression in ATDC5 cells was silenced by transfecting with miR-124 inhibitor, and the pro-inflammatory cytokines and Cox-2 were reassessed. NF-jB and JNK pathways were measured through western blot. Results: IL-1b stimulation accelerated the release of IL-1b, IL-6 and TNF-a, elevated Cox-2 expression. LBP significantly eased IL-1b-induced inflammation. MiR-124 expression was observed to enhance by LBP, and the impacts of LBP on ATDC5 cells were lightened via transfection with miR-124 inhibitor. NF-jB and JNK pathways were activated after IL-1b stimulation, nevertheless were inactivated by LBP administration. Besides, LBP-evoked the repression of NF-jB and JNK pathways were overturned by miR-124 inhibitor. Conclusions: Our study suggests that LBP protects ATDC5 cells from IL-1b-evoked injury through upregulating miR-124 via blocking NF-jB and JNK pathways.

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Section: Discussionsupporting

confidence: 61%

RETRACTED ARTICLE: Lycium barbarum polysaccharide alleviates IL-1β-evoked chondrogenic ATDC5 cell inflammatory injury through mediation of microRNA-124

Wang

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…Furthermore, the IL‐1β‐induced downregulation of Collagen II could be ameliorated by BBR. This result is consistent with previous studies (Huang et al, ). Moreover, MAPK signaling was evaluated to clarify the anti‐catabolic and anti‐inflammatory mechanisms; the results showed that BBR can suppress the ability to decrease the production of inflammation‐associated proteins through the MAPK signal pathway.…”

Section: Discussionsupporting

confidence: 94%

Berberine inhibits the interleukin‐1 beta‐induced inflammatory response via MAPK downregulation in rat articular chondrocytes

Hou

et al. 2019

Drug Development Research

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Osteoarthritis (OA) is one of the most chronic degenerative arthritic diseases, which gradually results in chondrocyte changes, articular cartilage degeneration, subchondral bone sclerosis, joint pain, swelling, and dysfunction. Berberine (BBR) has various confirmed biological activities, such as anti-inflammatory and antioxidant activities. However, the effect of BBR on the production of inflammation-associated proteins, including inducible nitric oxide synthase (iNOS), cyclooxygenase (Cox)-2, metalloproteinases (MMPs), Collagen II, TNF-α, and IL-6 via the MAPK (mitogenactivated protein kinases) pathway in IL-1β-stimulated rat chondrocytes, has not yet been studied. Thus, the purpose of this study was to evaluate whether BBR would decrease the production of inflammation-associated proteins through the MAPK signal pathway. Rat chondrocytes were cultured and pretreated with BBR at different concentrations (0, 25, 50, and 100 μM) and then stimulated with or without IL-1β (10 ng/mL). The mRNA expression of iNOS, COX-2, MMP-3, MMP-13, TNF-α, and IL-6 was measured by real-time polymerase chain reaction (RT-PCR), and the protein expression of iNOS, COX-2, Collagen II, MMP-3,MMP-13, and MAPKs were measured by Western blotting. The results showed that the expression of iNOS, COX-2, MMP-3, MMP-13, TNF-α, and IL-6 increased in the IL-1β-treated group and BBR showed an ability to inhibit the elevated expression under the pretreatment. Furthermore, the IL-1β-induced downregulation of Collagen II could be ameliorated by BBR.Moreover, the expression of MAPKs was significantly decreased by BBR. These results demonstrated that BBR had the anti-catabolic and anti-inflammation abilities that were through the MAPKs in IL-1β-induced rat chondrocytes. These findings may provide a novel therapeutic choice for treatment of OA using BBR. K E Y W O R D S berberine, chondrocyte, IL-1β, MAPKs, osteoarthritis Xing Li and Peiheng He contributed equally to this study.

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“…However, it seems that sinapic acid does not act on the same pathway in all cells. In human hair follicle dermal papilla cells, sinapic acid induces AKT activation and promotes hair growth [32], whereas in rat chondrocytes, sinapic acid inhibits IL-1β induced MAPK, thereby reducing inflammation [33]. ese data indicate that the mechanism of sinapic acid varies from cell to cell.…”

Section: Discussionmentioning

confidence: 98%

Sinapic Acid Promotes Browning of 3T3-L1 Adipocytes via p38 MAPK/CREB Pathway

Bae

Kim

2020

BioMed Research International

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Sinapic acid is a plant-derived phenolic compound, which acts as an antioxidant, anticancer, and anti-inflammatory agent. Although sinapic acid is valuable in a variety of therapeutic applications, its role in the improvement of obesity-related metabolic disease is relatively unexplored. Brown-like adipocytes (beige adipocytes) are characterized by a high concentration of mitochondria and high expression of uncoupling protein 1 (UCP1), which has specific functions in energy expenditure and thermogenesis. This study assessed the browning effects of sinapic acid in 3T3-L1 adipocytes. We investigated the expression of beige marker genes in 3T3-L1 adipocytes treated with sinapic acid. Sinapic acid increased the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α) and UCP1. Sinapic acid also promoted mitochondrial biogenesis by dose-dependently upregulating the oxygen consumption rate and enhancing the expression of representative subunits of oxidative phosphorylation complexes. In addition, treatment with p38 mitogen-activated protein kinase (MAPK) inhibitor and cAMP response element binding (CREB) inhibitor decreased the expressions of genes associated with thermogenesis, mitochondrial biogenesis, and oxidative phosphorylation. In summary, sinapic acid initiates browning 3T3-L1 adipocytes via the p38 MAPK/CREB signaling pathway. Thus, sinapic acid may have potential therapeutic implication in obesity.

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Sinapic Acid Inhibits the IL-1β-Induced Inflammation via MAPK Downregulation in Rat Chondrocytes

Cited by 33 publications

References 26 publications

RETRACTED ARTICLE: Lycium barbarum polysaccharide alleviates IL-1β-evoked chondrogenic ATDC5 cell inflammatory injury through mediation of microRNA-124

RETRACTED ARTICLE: Lycium barbarum polysaccharide alleviates IL-1β-evoked chondrogenic ATDC5 cell inflammatory injury through mediation of microRNA-124

Berberine inhibits the interleukin‐1 beta‐induced inflammatory response via MAPK downregulation in rat articular chondrocytes

Sinapic Acid Promotes Browning of 3T3-L1 Adipocytes via p38 MAPK/CREB Pathway

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