Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation

Ma, Zhiqiang; Piao, Taikui; Wang, Yanlong; Liu, Jianyu

doi:10.1016/j.intimp.2015.01.018

Cited by 70 publications

(47 citation statements)

References 33 publications

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“…Stimulating chondrocytes by IL-1β has been shown to induce phosphorylation and activation of ERK1/2, JNK, and p38 MAPKs [17]. In our study, enhanced expression of MAPK pathway proteins JNK, ERK and p38 were observed following IL-1β which is similar to the results of previous studies [10,17]. Nobiletin down-regulated the MAPK activation as evidenced by significant decrease in the expression of JNK, ERK and p38.…”

Section: Discussionsupporting

confidence: 91%

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Nobiletin Inhibits Expression of Inflammatory Mediators and Regulates JNK/ERK/p38 MAPK and PI3K/Akt Pathways in Human Osteoarthritic Chondrocytes

Liu¹,

Chong-wei²,

Wang³

et al. 2016

Trop. J. Pharm Res

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Section: Discussionsupporting

confidence: 91%

“…Astragalin, a bioactive component from Rosa agrestis [10] and piperine derived from Piper nigrum exhibited antiinflammatory effects in OA model [11]. In our study, we investigated the effects of nobiletin in IL-1β-induced OA.…”

Section: Osteoarthritismentioning

confidence: 99%

Nobiletin Inhibits Expression of Inflammatory Mediators and Regulates JNK/ERK/p38 MAPK and PI3K/Akt Pathways in Human Osteoarthritic Chondrocytes

Liu¹,

Chong-wei²,

Wang³

et al. 2016

Trop. J. Pharm Res

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“…Similarly, Zhu et al have observed an increase in the transcription of NF-κB and an association between the increased NF-κB expression and an increased level of IL-1β [23]. Thus, these results show the persistence of the effect of NF-κB on IL-1β [24,25].…”

Section: Discussionsupporting

confidence: 65%

Arsenic Trioxide Attenuates NF-κB and Cytokine mRNA Levels in the Livers of Cocks

Zhang

Zhao

Guo

et al. 2015

Biol Trace Elem Res

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Arsenic (As) is a trace element widely found in nature. It exists in several forms, including organic arsenic, inorganic arsenic, and trivalent arsenic, the most toxic. Arsenic trioxide (As2O3) is widespread in nature. This form tends to accumulate in animals and humans and therefore has a potential harm for them. Cytokines play essential roles in the immune response and inflammation. Although the importance of cytokines in the responses to arsenic exposure has been demonstrated in many types of mammals, the function of these in poultry, especially in chickens, remains unclear. The purpose of the present study was to examine the effect of As2O3 exposure on cytokines in cock livers. In this study, 72 1-day-old male Hy-line cocks were randomly divided into four groups including the control group, low-As group, middle-As group, and high-As group. The livers were collected on days 30, 60, and 90 of the experiment. The levels of nuclear factor-kappa B (NF-κB), tumor necrosis factor-alpha (TNF-α), interleukin-4 (IL-4), interleukin-6 (IL-6), interleukin-8 (IL-8), interleukin-12 beta (IL-12β), and interleukin-1 beta (IL-1β) mRNA in the livers of the cocks were measured using real-time PCR. The results showed that the expression levels of IL-6, IL-8, TNF-α, and NF-κB which seemed to be a critical mediator in the inflammatory response tended to increase in the birds chronically treated with As2O3. However, the mRNA expression levels of IL-4, IL-12β, and IL-1β were decreased in the experiment. The information regarding the effects of As2O3 on cytokine mRNA expression generated in this study will be important information for arsenic toxicology evaluation.

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“…As a result, TNF-α becomes a factor reflecting the activity and severity of RA. IL-1β, another inflammatory mediator, is secreted by monocyte-macrophages, and can induce synovial and cartilage cells to produce collagenase and PGE2, which leads to inflammation of the synovium and disintegration of the mesochondrium (16). At the same time, PGE2 can stimulate neutrophil, macrophage and lymphocyte aggregation in the articular cavity so that the arthritis will be exacerbated, which is a vicious cycle.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of higenamine ameliorates collagen-induced arthritis through heme oxygenase-1 and PI3K/Akt/Nrf-2 signaling pathways

Duan

Chen

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. Existing in Ranunculaceae Aconitum and tomato, with the chemical name 1-phydroxybenzyl-1,2,3,4-tetrahydroisoquinoline, higenamine is widely distributed in China. Higenamine's anti-inflammatory, antioxidant and anti-apoptotic effects have been identified in previous studies. The present study attempted to determine the protective effect of higenamine against collagen-induced arthritis through heme oxygenase-1 (HO-1) and PI3K/Akt/Nrf-2 signaling pathways. A type II collagen (CII)-induced arthritis (CIA) model was established and clinical arthritis scores were used to appraise the curative effect of higenamine. Inflammatory reactions, oxidative damage and caspase-3/9 activation were detected using specific ELISA kits. In addition, western blotting was used to evaluate the expression of HO-1, Akt and Nrf-2 protein in CII-induced CIA mice. In CII-induced CIA mice, the clinical arthritis scores, inflammatory reactions, oxidation damage and caspase-3/9 activation were increased and activated. The results demonstrated that treatment with higenamine significantly reduced the elevation of clinical arthritis scores (P<0.01), and suppressed the promotion of inflammatory reactions, oxidation damage and caspase-3/9 activation. Furthermore, higenamine significantly increased HO-1 protein expression (P<0.01) and upregulated the PI3K/Akt/Nrf-2 signal pathway in CII-induced CIA mice. Collectively, it is concluded that higenamine protects against CII-induced CIA through the induction of HO-1 and the upregulation of the PI3K/Akt/Nrf-2 signaling pathway. In conclusion, higenamine may be a beneficial drug for protecting against CIA.

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Astragalin inhibits IL-1β-induced inflammatory mediators production in human osteoarthritis chondrocyte by inhibiting NF-κB and MAPK activation

Cited by 70 publications

References 33 publications

Nobiletin Inhibits Expression of Inflammatory Mediators and Regulates JNK/ERK/p38 MAPK and PI3K/Akt Pathways in Human Osteoarthritic Chondrocytes

Nobiletin Inhibits Expression of Inflammatory Mediators and Regulates JNK/ERK/p38 MAPK and PI3K/Akt Pathways in Human Osteoarthritic Chondrocytes

Arsenic Trioxide Attenuates NF-κB and Cytokine mRNA Levels in the Livers of Cocks

Protective effect of higenamine ameliorates collagen-induced arthritis through heme oxygenase-1 and PI3K/Akt/Nrf-2 signaling pathways

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