Pharmacological Effect of <i>Caulophyllum robustum</i> on Collagen‐Induced Arthritis and Regulation of Nitric Oxide, NF‐<i>κ</i>B, and Proinflammatory Cytokines In Vivo and In Vitro

Wang, Qiuhong; Lv, Shaowa; Guo, Yuan‐ji; Duan, Ji-Xin; Dong, Shuyu; Wang, Qiushi; Yu, Feng-Ming; Su, Hong; Kuang, Hai‐Xue

doi:10.1155/2017/8134321

Cited by 30 publications

(5 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Rheumatoid arthritis affects the function of joints and tissues, which may lead to various pathological symptoms, including fatigue, general discomfort and body weight loss (34). A previous study has demonstrated that NF-κB and various pro-inflammatory cytokines are involved in the inflammation of the joints through multiple signaling pathways both in vivo and in vitro (35). In the present study, the role of the pro-inflammatory cytokine IL-1β was investigated in vitro , using sfd-FLSs, and in vivo , using a rat model of rheumatoid arthritis.…”

Section: Discussionmentioning

confidence: 99%

IL‑1β increases the expression of inflammatory factors in synovial fluid‑derived fibroblast‑like synoviocytes via activation of the NF‑κB‑mediated ERK‑STAT1 signaling pathway

et al. 2019

View full text Add to dashboard Cite

Interleukin (IL)-1β serves a crucial role in the progression of rheumatoid arthritis. Previous studies have indicated that the ERK/STAT1 signaling pathway may be involved in the inflammatory response in synovial fluid-derived fibroblast-like synoviocytes (sfd-FLSs). However, the molecular mechanisms underlying the pathological effects of the inflammatory factors induced by IL-1β in sfd-FLSs remain unclear. The aim of the present study was to investigate the IL-1β-mediated signaling pathways involved in the expression of inflammatory factors in sfd-FLSs and in a rat model of rheumatoid arthritis. Reverse transcription-quantitative PCR, western blotting, and immunohistochemistry were used to analyze the role of IL-1β in the rat model of rheumatoid arthritis. The results suggested that IL-1β administration exacerbated rheumatoid arthritis, bone injury and increased the expression levels of inflammatory factors, such as IL-17 and tumor necrosis factor α (TNF-α), whereas treatment with anti-IL-1β exhibited opposite effects. In vitro experiments in sfd-FLSs further suggested that treatment with IL-1β influenced the expression levels of various inflammatory factors. In specific, IL-1β increased the expression of IL-17 and TNF-α, and decreased the expression of IL-6 and IL-10 in sfd-FLSs. Additionally, treatment with IL-1β increased the mRNA expression and protein phosphorylation of NF-κB, ERK and STAT1 in sfd-FLSs. Treatment with anti-IL-1β exhibited opposite effects on the expression levels of inflammatory factors and suppressed the NF-κB-mediated ERK-STAT1 signaling pathway activation in sfd-FLSs. Finally, treatment with a NF-κB inhibitor suppressed the effects of IL-1β, and NF-κB overexpression reversed the effects of anti-IL-1β on the expression levels of IL-17, TNF-α, NF-κB, ERK and STAT1. In conclusion, the present results demonstrated that treatment with IL-1β increased the expression levels of inflammatory factors in sfd-FLSs via the regulation of the NF-κB-mediated ERK/STAT1 signaling pathway in a rat model of rheumatoid arthritis. Therefore, the NF-κB/ERK/STAT1 signaling pathway may represent a potential target for the development of novel treatments for rheumatoid arthritis.

show abstract

Section: Discussionmentioning

confidence: 99%

IL‑1β increases the expression of inflammatory factors in synovial fluid‑derived fibroblast‑like synoviocytes via activation of the NF‑κB‑mediated ERK‑STAT1 signaling pathway

et al. 2019

View full text Add to dashboard Cite

show abstract

“…From day 24, the thickness of the hind paws of mice was measured with Vernier calipers every 4 days. The inflammatory scores of all four paws were assessed using the following methods: 0 = normal; 1 = erythema or slight swelling in the ankle joints; 2 = erythema and slight swelling from the ankle joints-to-the toe or metacarpal joints; 3 = erythema and moderate swelling from the ankle joints-to-the toe or metacarpal joints; and 4 = erythema and severe swelling from the ankle joints-to-the toe or metacarpal joints (18). The score for each mouse was the sum of four paws; the minimum score was 0, and the maximum score was 16.…”

Section: Paw Thickness Measurement and Arthritic Index Scoringmentioning

confidence: 99%

Characteristics of Ang-(1–7)/Mas-Mediated Amelioration of Joint Inflammation and Cardiac Complications in Mice With Collagen-Induced Arthritis

et al. 2021

View full text Add to dashboard Cite

ObjectivesRheumatoid arthritis (RA) is a disabling disease with a high incidence that is regularly accompanied by cardiovascular complications. Several studies have suggested that renin–angiotensin–aldosterone system (RAAS) is closely associated with RA. The aim of this study was to investigate the mechanisms underlying Angiotensin-(1–7) [Ang-(1–7)] and its Mas receptor agonist (AVE0991) on joint inflammation and cardiac complications in a collagen-induced arthritis (CIA) model.MethodsCollagen type II was injected into DBA/1 mice to construct an arthritis model. CIA mice were treated with Ang-(1–7) (2.0 mg/kg intraperitoneally) and AVE0991 (3.0 mg/kg intraperitoneally). The serum levels of inflammatory cytokines [tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1 β, IL-6, and C-reactive protein (CRP)] were determined by ELISA. The mitogen-activated protein kinase (MAPK) and nuclear factor-kappaB (NF-κB) signaling pathways in joint tissues and the transforming growth factor (TGF)-β/Smad pathway and levels of α-Smooth muscle action (SMA) and β-myosin heavy chain (MHC) protein expression in cardiac tissues were assessed by western blots. The levels of TGF-β/Smad pathway, α-SMA, and β-MHC RNA in cardiac tissues were analyzed by real time-PCR. The levels of receptor activator of nuclear factor kappa ligand (RANKL) and promoting matrix metalloproteinase (MMP)-3 expression in the ankle joints were detected by immunohistochemistry and real time-PCR.ResultsAng-(1–7) and AVE0991 reduced the levels of inflammatory cytokines and inhibited the MAPKs and NF-κB signaling pathways in ankle joint tissues, reduced RANKL and MMP3 expression, and ameliorated local joint inflammation and bone destruction compared with the control group. In addition, Ang-(1–7) and AVE0991 attenuated the TGF-β/Smad signaling pathway, reduced the levels of α-SMA and β-MHC expression, and diminished inflammatory cell infiltration into the myocardial interstitium and myocardial interstitial fibrosis in the hearts of CIA mice.ConclusionsAng-(1–7) alleviated joint damage caused by inflammation likely through the attenuation of NF-κB and MAPK pathways and ameliorated inflammation-induced cardiac fibrosis and activation of the TGF-β/Smad pathway. Moreover, Ang-(1–7) was likely mediated through the Mas receptor. This study provides theoretical evidence for exploring novel clinical therapeutic approaches for RA and its cardiac complications.

show abstract

“…It is widely believed that TNF-a plays an important role in the pathogenesis of inflammatory arthritis (15). The collagen-induced arthritis (CIA) mouse model and the collagen antibody-induced arthritis (CAIA) mouse model are often used in RA research (16,17), and macrophages can be investigated in these models (18,19).…”

mentioning

confidence: 99%

GDF11 antagonizes TNF‐α‐induced inflammation and protects against the development of inflammatory arthritis in mice

Wang

Liu

et al. 2018

FASEB j.

View full text Add to dashboard Cite

Growth differentiation factor 11 (GDF11), a key member of the TGF‐β superfamily, plays critical roles in various medical conditions. Recently, GDF11 was found to suppress the nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB) signaling pathway and protect against inflammation. This study aimed to investigate the role of GDF11 in the development of rheumatoid arthritis (RA). We demonstrated that GDF11 treatment antagonized TNF‐α‐induced inflammation in macrophages. Moreover, GDF11 inhibited the development of arthritis in the collagen‐induced arthritis and collagen antibody‐induced arthritis models. Local gene transfer of GDF11 via adeno‐associated virus exerted therapeutic effects, while local knockdown of GDF11 exaggerated inflammation in our collagen‐induced arthritis model, as detected by expression levels of inflammatory biomarkers and the destruction of joint structures. Additionally, the results from both in vitro experiments and luciferase reporter gene mouse experiments implied that the NF‐κB pathway might play a critical role in the therapeutic effect of GDF11 in RA. This study presents GDF11 as a potential target for the treatment of inflammatory arthritis, including RA.—Li, W., Wang, W., Liu, L., Qu, R., Chen, X., Qiu, C., Li, J., Hayball, J., Liu, L., Chen, J., Wang, X., Pan, X., Zhao, Y. GDF11 antagonizes TNF‐α‐induced inflammation and protects against the development of inflammatory arthritis in mice. FASEB J. 33, 3317–3329 (2019). http://www.fasebj.org

show abstract

Pharmacological Effect of Caulophyllum robustum on Collagen‐Induced Arthritis and Regulation of Nitric Oxide, NF‐κB, and Proinflammatory Cytokines In Vivo and In Vitro

Cited by 30 publications

References 26 publications

IL‑1β increases the expression of inflammatory factors in synovial fluid‑derived fibroblast‑like synoviocytes via activation of the NF‑κB‑mediated ERK‑STAT1 signaling pathway

IL‑1β increases the expression of inflammatory factors in synovial fluid‑derived fibroblast‑like synoviocytes via activation of the NF‑κB‑mediated ERK‑STAT1 signaling pathway

Characteristics of Ang-(1–7)/Mas-Mediated Amelioration of Joint Inflammation and Cardiac Complications in Mice With Collagen-Induced Arthritis

GDF11 antagonizes TNF‐α‐induced inflammation and protects against the development of inflammatory arthritis in mice

Contact Info

Product

Resources

About