Inflammation and intracellular metabolism: new targets in OA

Liu‐Bryan, Ru

doi:10.1016/j.joca.2014.12.016

Cited by 84 publications

(65 citation statements)

References 114 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As stated in the introduction, pathophysiology of OA is very complex due to involvement of multiple factors [18,[20][21][22][23][24][25][26]. Among all these factors, oxidative stress (due to excess generation of free radicals) and inflammation are proven to be the major contributing factors in joint damage and pain [67][68][69][70][71].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Terminalia chebula Extract for Anti-Arthritic Efficacy and Safety in Osteoarthritic Dogs

Murdock¹,

Vega³

et al. 2015

J Veterinar Sci Technol

View full text Add to dashboard Cite

The present investigation was undertaken to assess anti-inflammatory and anti-arthritic efficacy and safety of T. chebula extract (TCE) in moderately osteoarthritic (OA) dogs. Dogs with OA received either 500 mg placebo or 500 mg TCE twice daily for 150 days. On a monthly basis, dogs were given a full physical exam and were evaluated for arthritic pain (overall pain, pain upon limb manipulation, and pain after physical exertion), inflammation (erythrocyte sedimentation rate, ESR), and analysis of complete blood count (CBC) and serum biomarkers of liver (bilirubin, ALT, and AST), kidney (BUN and creatinine), and heart and skeletal muscle (CK) functions. Elbow and stifle joints were radiographed on day 0 and day 150 for evaluation of arthritic progression. Dogs given TCE showed significant (P<0.01) reductions in overall pain, pain upon limb manipulation, and pain after physical exertion by day 90, with maximum effects on day 150 (81.2%, 81.5%, and 84.2%, respectively). A marked reduction in ESR coincided with pain reduction in TCE-treated dogs, which was indicative of anti-inflammatory effect of TCE. Radiographic evidence also indicated slowed progression of OA in joints examined. No significant change occurred in physical parameters, CBC parameters, or serum biomarkers in dogs on placebo or treatment, which suggested that TCE was well tolerated. It can be concluded that TCE, by having many active principles (chebulagic acid, chebulinic acid, corilagin, hydrolysable tannoids, etc.) might have provided antioxidant, anti-inflammatory and anti-arthritic effects in dogs without causing any side effects.

show abstract

Section: Discussionmentioning

confidence: 99%

Evaluation of Terminalia chebula Extract for Anti-Arthritic Efficacy and Safety in Osteoarthritic Dogs

Murdock¹,

Vega³

et al. 2015

J Veterinar Sci Technol

View full text Add to dashboard Cite

show abstract

Section: Introductionmentioning

confidence: 99%

“…Progressive degeneration of articular cartilage is a common feature of osteoarthritis (OA) [3,4]. OA is the most prevalent joint disease and has a complex pathogenesis and pathophysiology [4][5][6]. The effects of mechanical force acting on articular cartilage, obesity, inflammation and aging are among the major catabolic factors in OA, suggesting that both extrinsic and intrinsic stresses acting on articular cartilage matrix and chondrocytes are both causal and contributory factors to the catabolic process in OA [5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

“…It is well known that MMP-13 contributes to OA cartilage degradation [3][4][5]. The expression level of MMP-13 is significantly higher in the chondrocytes of advanced stage OA cartilage in comparison with early OA or normal knee cartilage [28].…”

Section: Introductionmentioning

confidence: 99%

“…The OA-related catabolic factor IL-1β alters chondrocyte activity and induces chondrocyte apoptosis [4][5][6][7][8]. However, few studies have examined how the catabolic cytokine impacts chondrocyte energy metabolism in articular cartilage.…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Nicotinamide Adenine Dinucleotide (NAD)-Dependent Deacetylase Sirtuin-1 Regulates Chondrocyte Energy Metabolism through the Modulation of Adenosine Monophosphate-Activated Protein Kinase (AMPK) in Osteoarthritis(OA)

Kobayashi¹,

Terauchi²,

Yui³

et al. 2017

J Arthritis

View full text Add to dashboard Cite

To clarify how the osteoarthritis (OA)-induced catabolic factor interleukin (IL)-1β affects chondrocyte energy metabolism, and especially to define the downstream pathway linking nicotinamide adenine dinucleotide (NAD)-dependent deacetylase Sirtuin-1 (Sirt-1) to energy metabolism in OA chondrocytes. Human chondrocytes were isolated from articular cartilage samples of patients with OA. The level of energy metabolism of OA chondrocytes was evaluated by monitoring the activity of the energy metabolic sensor, adenosine monophosphate-activated protein kinase (AMPK) and the level of production of adenosine triphosphate (ATP) in chondrocytes in the presence or absence of t IL-1β (10 ng/mL). Effects of IL-1β on anabolic and catabolic activities of chondrocytes were analyzed by the levels of production of proteoglycan and matrix metalloproteinase (MMP)-13, respectively. Experiments involving pre-treatment with Sirt-1 inhibitor were also performed to investigate the underlying regulatory mechanism linking Sirt-1 to chondrocyte energy metabolism. IL-1β significantly inhibited the activity of AMPK and production of ATP in OA chondrocytes. The energy metabolism disruption mediated by IL-1β was further decreased by pretreatment with Sirt-1 inhibitor in OA chondrocytes. Treatment with IL-1β significantly decreased the level of proteoglycan production and significantly increased the level of MMP-13 secretion by chondrocytes. These chondrocyte activities were also reduced by pre-treatment with the Sirt-1 inhibitor in OA chondrocytes. IL-1β inhibits the AMPK -ATP energy metabolic pathway in OA chondrocytes. Our findings also suggest that Sirt-1 activity is involved in anabolic and catabolic cellular activities and that Sirt-1 modulates ATP production through functional regulation of the energy sensor AMPK in chondrocytes.

show abstract