Ankylosing spondylitis with idiopathic spinal cord herniation

Gao, Hongxiang; Xue-ju, LI; Wang, Cunping

doi:10.1016/j.spinee.2014.10.024

Cited by 5 publications

(4 citation statements)

References 3 publications

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“…1,2 AS would progress to functional and structural impairments, which greatly reduce the life quality. 3 In the drug therapy of AS, nonsteroidal anti-inflammatory drugs (NSAIDs) are the first choice. Other anti-TNFα agents are also preferable.…”

Section: Introductionmentioning

confidence: 99%

“…Ankylosing spondylitis (AS) is an autoimmune disease, which is characterized by pathological bone formation, inflammatory back stiffened, and pain . AS would progress to functional and structural impairments, which greatly reduce the life quality . In the drug therapy of AS, nonsteroidal anti‐inflammatory drugs (NSAIDs) are the first choice.…”

Section: Introductionmentioning

confidence: 99%

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Effect of metformin on ossification and inflammation of fibroblasts in ankylosing spondylitis: An in vitro study

Xiong

Jiang

Liu

et al. 2017

J of Cellular Biochemistry

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Ankylosing spondylitis (AS) is an autoimmune disease characterized by fibroblasts ossification. However, effective drug therapy for AS is lacking. As an antidiabetic drug, metformin has demonstrated an antiosteogenic effect on osteoblasts in vitro. And it is also a kind of specific agonists for adenosine 5′-monophosphate activated protein kinase (AMPK), which is blocked in the process of AS. Given the role in antiosteogenesis and AMPK activating, metformin was investigated of its effect on fibroblasts harvested from capsular ligament of patients with femoral neck fracture and AS. Osteogenic specific makers (Alp, Bglap, Runx2, Bmp2, and Col1) in fibroblasts administered with metformin (20 μg/mL) were detected by ALP staining, alizarin red staining, qPCR, and Western blotting after 7 and 14 days of culture. Inflammation genes (il1-β and il6) and pathway (Pi3k, Akt, and Ampk) associated markers were also evaluated. Our results showed that osteogenic specific markers were greatly downregulated and ossification was effectively inhibited in AS fibroblasts after addition of metformin. Levels of inflammation markers were also decreased by metformin. Thus, metformin exerts potent effect on suppression of ossification and inflammation in AS fibroblasts via the activation of Pi3k/Akt and AMPK pathways, which may be developed as a potential agent for treatment of AS. K E Y W O R D Sankylosing spondylitis, fibroblasts, metformin, ossification Xiong Qin, Tongmeng Jiang, and Sijia Liu contributed equally to this work.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effect of metformin on ossification and inflammation of fibroblasts in ankylosing spondylitis: An in vitro study

Xiong

Jiang

Liu

et al. 2017

J of Cellular Biochemistry

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“…The occurrence of AS is insidious and progressive, and the major clinical manifestations of the early stage are joint pain without apparent cause, which is easily ignored by patients, leading to missed diagnosis and delay in treatment. Advanced AS may lead to spinal deformity, loss of ability to work, and disability, seriously affecting the quality of life [ 8 – 11 ]. The prevalence of AS in China is about 0.20% to 0.40% [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Protective Effects of Sinomenine Against Ankylosing Spondylitis and the Underlying Molecular Mechanisms

Dong

2018

Med Sci Monit

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BackgroundThis study aimed to investigate the effect and underlying molecular mechanism of sinomenine (SIN) on ankylosing spondylitis (AS).Material/MethodsTo study the potential role of SIN in the pathogenesis of AS, an AS mouse model was established and mice were treated with different concentrations of SIN (10, 30, and 50 mg/kg, administered intraperitoneally). Markers of inflammation and oxidative stress were determined by ELISA assay. Western blot analysis and qRT-PCR were used to quantify the levels of related proteins and gene mRNA expression.ResultsThe results suggest that AS mice has higher levels of TNF-α, IL-1β, and IL-6 (p<0.01 for all), and lower levels of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-PX) (p<0.01 for all). SIN treatment reduced the level of TNF-α, IL-1β, and IL-6 in a dose-dependent manner, and the levels of SOD, CAT, and GSH-PX were dose-dependently increased (p<0.05 for all). The results also revealed that NF-κBp65 expression decreased, while the level of IκB increased, in a dose-dependent manner, after SIN treatment in AS mice (p<0.05 for all). The level of p-p38 was dose-dependently reduced in AS mice by SIN treatment (p<0.05). Moreover, SIN inhibited Cox-2 expression in AS mice in a dose-dependent manner (p<0.05).ConclusionsSIN has a beneficial role in AS through suppressing inflammatory mediators and by down-regulating oxidative stress via inhibiting the MAPKp38/NF-κB pathway and Cox-2 expression.

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“…1–6 It can lead to functional and structural impairments and reduction in quality of life. 7–10 The prevalence of AS is about 0.20% to 0.40% in China. 11–13 Almost 80% of AS influences young adults and the disability rate after 5 years of symptoms onset reaches 40% to 60%.…”

Section: Introductionmentioning

confidence: 99%

The Role of MicroRNAS in Ankylosing Spondylitis

Wong

Shen

et al. 2016

Medicine

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Ankylosing spondylitis (AS) is a common and genetically heterozygous inflammatory rheumatic disease characterized by new bone formation, ankylosis and inflammation of hip, sacroiliac joints and spine. Until now, there is no method for early diagnosis of AS and the effective treatment available for AS patients remain largely undefined.We searched articles indexed in PubMed (MEDLINE) database using Medical Subject Heading (MeSH) or Title/Abstract words (“microRNA” and “ankylosing spondylitis”) from inception up to November 2015.Genetic polymorphisms of miRNAs and their targets might alter the risk of AS development whereas certain miRNAs exhibit correlation with inflammatory index.Let-7i and miR-124 were upregulated whereas miR-130a was downregulated in circulating immune cells of AS patients. These deregulated miRNAs could modulate key immune cell functions, such as cytokine response and T-cell survival.miRNA deregulation is key to AS pathogenesis. However, clinical utilization of miRNAs for management of AS patients requires further support from future translational studies.

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Ankylosing spondylitis with idiopathic spinal cord herniation

Cited by 5 publications

References 3 publications

Effect of metformin on ossification and inflammation of fibroblasts in ankylosing spondylitis: An in vitro study

Effect of metformin on ossification and inflammation of fibroblasts in ankylosing spondylitis: An in vitro study

Protective Effects of Sinomenine Against Ankylosing Spondylitis and the Underlying Molecular Mechanisms

The Role of MicroRNAS in Ankylosing Spondylitis

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