COX-2, NO, and cartilage damage and repair

2000 ◽  
Vol 2 (6) ◽  
pp. 447-453 ◽  
Author(s):  
Ashok R. Amin ◽  
Mandar Dave ◽  
Mukundan Attur ◽  
Steven B. Abramson
Keyword(s):  
Cox 2 ◽  
QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Samer Mohamed Moustafa ◽  
Amany Moh. Rashad Abdel-Aziz ◽  
Mennatallah Hatem Shalaby

Abstract Background Using MRI, ACL mucoid degeneration is defined as a thickened ACL with increased signal intensity on all MR pulse sequences, with discrete fibers easily distinguished on fatsaturated T2-weighted or fat-saturated proton-density (PD)-weighted images but poorly differentiated on T1-weighted or non-fat-saturated PD-weighted images. Objective To assess the prevalence of ACL mucoid degeneration in a population of patients referred for routine knee MRI, and its association with age and structural joint damage. Patients and Methods Our study is a retrospective study conducted at the radiology department of Ain Shams University hospitals and Ain Shams University Specialized Hospital including 81 cases of knees with ACL mucoid degeneration by MRI and no sex predilection. Cases and controls were scored with respect to independent articular features: cartilage signal and morphology, subarticular bone marrow abnormality, subarticular cysts, subarticular bone attrition, marginal osteophytes and medial meniscal integrity. Results Patients with ACL mucoid degeneration were older than patients with a normal ACL, without statistically significant sex difference. Knees with ACL mucoid degeneration had statistically significant medial meniscal injuries and cartilage damage involving the central and posterior MTFC compared to control knees with a normal ACL frequency matched for age, sex and MR field strength. Conclusion Our study proved that there is a strong association between ACL mucoid degeneration and cartilage damage in MTFC.


2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Yu Chen ◽  
Jiuheng Lv ◽  
Yejuan Jia ◽  
Ruiqing Wang ◽  
Zidi Zhang ◽  
...  

In this study, a knee osteoarthritis (KOA) rat model induced by monosodium iodoacetate (MIA) was used to study the effect of moxibustion on improving knee cartilage damage and its effect on the intestinal flora. The experimental rats were divided into the normal group (N), model group (M), moxibustion treatment group (MS), and diclofenac sodium treatment group (DS). After 4 weeks, cartilage pathological damage in the knee joint was evaluated using hematoxylin-eosin and safranin O-fast green staining analysis. ELISAs and Western blots were used to detect the expression levels of IL-1β and TNF-α in the serum and cartilage, respectively. The total DNA of the fecal samples was extracted and subjected to high-throughput sequencing of the V3-V4 region of the 16S rRNA gene to analyze the changes in the intestinal flora. In the model group, the cartilage was obviously damaged, the expression levels of IL-1β and TNF-α in the serum and cartilage were increased, and the abundance and diversity of the intestinal flora were decreased. Moxibustion treatment significantly improved the cartilage damage and reduced the concentration of inflammatory factors in the serum and cartilage. The high-throughput sequencing results showed that compared to the model group, the moxibustion treatment regulated some specific species in the intestinal microorganisms rather than the α diversity. In conclusion, our findings suggest that moxibustion treatment may work through two aspects in rats. On one hand, it directly acts on knee cartilage to promote repair, and on the other hand, it regulates the composition of the intestinal flora and reduces the production of inflammatory factors.


2018 ◽  
Vol 77 (11) ◽  
pp. 1636-1643 ◽  
Author(s):  
Marta F Bustamante ◽  
Patricia G Oliveira ◽  
Ricard Garcia-Carbonell ◽  
Adam P Croft ◽  
Jeff M Smith ◽  
...  

ObjectivesRecent studies indicate that glucose metabolism is altered in rheumatoid arthritis (RA) fibroblast-like synoviocytes (FLS). Hexokinases (HKs) catalyse the first step in glucose metabolism, and HK2 constitutes the principal HK inducible isoform. We hypothesise that HK2 contributes to the synovial lining hypertrophy and plays a critical role in bone and cartilage damage.MethodsHK1 and HK2 expression were determined in RA and osteoarthritis (OA) synovial tissue by immunohistochemistry. RA FLS were transfected with either HK1 or HK2 siRNA, or infected with either adenovirus (ad)-GFP, ad-HK1 or ad-HK2. FLS migration and invasion were assessed. To study the role of HK2 in vivo, 108 particles of ad-HK2 or ad-GFP were injected into the knee of wild-type mice. K/BxN serum transfer arthritis was induced in HK2F/F mice harbouring Col1a1-Cre (HK2Col1), to delete HK2 in non-haematopoietic cells.ResultsHK2 is particular of RA histopathology (9/9 RA; 1/8 OA) and colocalises with FLS markers. Silencing HK2 in RA FLS resulted in a less invasive and migratory phenotype. Consistently, overexpression of HK2 resulted in an increased ability to migrate and invade. It also increased extracellular lactate production. Intra-articular injection of ad-HK2 in normal knees dramatically increased synovial lining thickness, FLS activation and proliferation. HK2 was highly expressed in the synovial lining after K/BxN serum transfer arthritis. HK2Col1 mice significantly showed decreased arthritis severity, bone and cartilage damage.ConclusionHK2 is specifically expressed in RA synovial lining and regulates FLS aggressive functions. HK2 might be an attractive selective metabolic target safer than global glycolysis for RA treatment.


Molecules ◽  
2020 ◽  
Vol 25 (22) ◽  
pp. 5467
Author(s):  
Hae Lim Kim ◽  
Hae Jin Lee ◽  
Dong-Ryung Lee ◽  
Bong-Keun Choi ◽  
Seung Hwan Yang

The aim of this study was to determine the anti-osteoarthritic effects of LI73014F2, which consists of Terminalia chebula fruit, Curcuma longa rhizome, and Boswellia serrata gum resin in a 2:1:2 ratio, in the monosodium iodoacetate (MIA)-induced osteoarthritis (OA) rat model. LI73014F2 was orally administered once per day for three weeks. Weight-bearing distribution and arthritis index (AI) were measured once per week to confirm the OA symptoms. Synovial membrane, proteoglycan layer, and cartilage damage were investigated by histological examination, while synovial fluid interleukin-1β level was analyzed using a commercial kit. Levels of pro-inflammatory mediators/cytokines and matrix metalloproteinases (MMPs) in the cartilage tissues were investigated to confirm the anti-osteoarthritic effects of LI73014F2. LI73014F2 significantly inhibited the MIA-induced increase in OA symptoms, synovial fluid cytokine, cartilage damage, and expression levels of pro-inflammatory mediators/cytokines and MMPs in the articular cartilage. These results suggest that LI73014F2 exerts anti-osteoarthritic effects by regulating inflammatory cytokines and MMPs in MIA-induced OA rats.


Author(s):  
Songyang Liu ◽  
Chenxi Cao ◽  
Yujun Zhang ◽  
Guangyu Liu ◽  
Weixia Ren ◽  
...  

Abstract Background The Cadherin-11 and PI3K/Akt pathway are increasingly recognized as the potential therapeutic target of osteoarthritis (OA) synovitis. The study aimed to investigate the role of PI3K/Akt signaling pathway in the expression of Cadherin-11 and migration and invasive capacity of fibroblast-like synoviocytes (FLS) of OA patients under stimulation of TNF-α and to explore the effect of the PI3K/Akt inhibitor and Cadherin-11 antibody in the therapy of the collagenase-induced osteoarthritis (CIOA) mice. Methods FLS were primarily cultured from synovium of osteoarthritic patients during total knee arthroplasty. Under the simulation of TNF-α, with or without PI3K/Akt inhibitor LY294002, Cadherin-11 expression was detected by real-time PCR and Western blot, as well as the migration and invasive capacity changes of OA FLS. Cadherin-11 antibody was injected intraarticularly or LY294002 was injected intraperitoneally in CIOA mice to evaluate the changes of synovitis score, cartilage damage, and Cadherin-11 expression. Results TNF-α stimulation increased Cadherin-11 expression at mRNA and protein level in OA FLS and also increased the phosphorylation-dependent activation of Akt. PI3K inhibitor LY294002 attenuated TNF-α-induced overexpression of Cadherin-11 and decreased the invasive capacity of OA FLS. Intraperitoneal injection of PI3K inhibitor LY294002 could decrease the Cadherin-11 protein expression in synovium of CIOA mice, although it has no significant inhibitory effect on synovitis and cartilage damage. Intraarticular injection of Cadherin-11 antibody attenuated the synovitis and cartilage damage in the CIOA joints and decreased Cadherin-11 expression in the synovial lining. Conclusions PI3K/Akt pathway was associated with TNF-α-induced activation of OA FLS, which may involve in the pathogenesis of osteoarthritis. Anti-Cadherin-11 therapy in CIOA mice could attenuate the pathological changes of OA joints.


2011 ◽  
Vol 63 (7) ◽  
pp. 937-944 ◽  
Author(s):  
K. Douglas Gross ◽  
David T. Felson ◽  
Jingbo Niu ◽  
David J. Hunter ◽  
Ali Guermazi ◽  
...  

2008 ◽  
Vol 36 (5) ◽  
pp. 934-942 ◽  
Author(s):  
Chen Hua Yeow ◽  
Chee Hoong Cheong ◽  
Kian Siang Ng ◽  
Peter Vee Sin Lee ◽  
James Cho Hong Goh

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