scholarly journals Honokiol Inhibits the Progression of Collagen-Induced Arthritis by Reducing Levels of Pro-inflammatory Cytokines and Matrix Metalloproteinases and Blocking Oxidative Tissue Damage

2010 ◽  
Vol 114 (1) ◽  
pp. 69-78 ◽  
Author(s):  
Ki Rim Kim ◽  
Kwang-Kyun Park ◽  
Kyung-Soo Chun ◽  
Won-Yoon Chung
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Cytokines ◽  
Tissue Damage ◽  
Collagen Induced Arthritis ◽  
Pro Inflammatory Cytokines

Cytokine synergy, collagenases and cartilage collagen breakdown

2003 ◽  
Vol 70 ◽  
pp. 125-133 ◽  
Author(s):  
Tim E. Cawston ◽  
Jenny M. Milner ◽  
Jon B. Catterall ◽  
Andrew D. Rowan
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Cytokines ◽  
Activator Protein 1 ◽  
Activator Protein ◽  
And Cartilage ◽  
Pro Inflammatory Cytokines

We have investigated proteinases that degrade cartilage collagen. We show that pro-inflammatory cytokines act synergistically with oncastatin M to promote cartilage collagen resorption by the up-regulation and activation of matrix metalloproteinases (MMPs). The precise mechanisms are not known, but involve the up-regulation of c-fos, which binds to MMP promoters at a proximal activator protein-1 (AP-1) site. This markedly up-regulates transcription and leads to higher levels of active MMP proteins.

Cinnamaldehyde and eugenol attenuates collagen induced arthritis via reduction of free radicals and pro-inflammatory cytokines

Phytomedicine ◽  
2019 ◽  
Vol 53 ◽  
pp. 70-78 ◽  
Author(s):  
Somaiya Mateen ◽  
Sumayya Shahzad ◽  
Shafeeque Ahmad ◽  
Syed Shariq Naeem ◽  
Saifullah Khalid ◽  
...  
Keyword(s):  
Free Radicals ◽  
Inflammatory Cytokines ◽  
Collagen Induced Arthritis ◽  
Pro Inflammatory Cytokines

scholarly journals Osteostatin Inhibits Collagen-Induced Arthritis by Regulation of Immune Activation, Pro-Inflammatory Cytokines, and Osteoclastogenesis

2019 ◽  
Vol 20 (16) ◽  
pp. 3845 ◽  
Author(s):  
Josep Nácher-Juan ◽  
María Carmen Terencio ◽  
María José Alcaraz ◽  
María Luisa Ferrándiz
Keyword(s):  
T Cells ◽  
Bone Loss ◽  
Inflammatory Cytokines ◽  
T Cell Activation ◽  
Immune Activation ◽  
Joint Destruction ◽  
Related Protein ◽  
Collagen Induced Arthritis ◽  
Parathyroid Hormone Related Protein ◽  
Pro Inflammatory Cytokines

In chronic inflammatory joint diseases, such as rheumatoid arthritis, there is an important bone loss. Parathyroid hormone-related protein (PTHrP) and related peptides have shown osteoinductive properties in bone regeneration models, but there are no data on inflammatory joint destruction. We have investigated whether the PTHrP (107-111) C-terminal peptide (osteostatin) could control the development of collagen-induced arthritis in mice. Administration of osteostatin (80 or 120 μg/kg s.c.) after the onset of disease decreased the severity of arthritis as well as cartilage and bone degradation. This peptide reduced serum IgG2a levels as well as T cell activation, with the downregulation of RORγt+CD4+ T cells and upregulation of FoxP3+CD8+ T cells in lymph nodes. The levels of key cytokines, such as interleukin(IL)-1β, IL-2, IL-6, IL-17, and tumor necrosis factor-α in mice paws were decreased by osteostatin treatment, whereas IL-10 was enhanced. Bone protection was related to reductions in receptor activator of nuclear factor-κB ligand, Dickkopf-related protein 1, and joint osteoclast area. Osteostatin improves arthritis and controls bone loss by inhibiting immune activation, pro-inflammatory cytokines, and osteoclastogenesis. Our results support the interest of osteostatin for the treatment of inflammatory joint conditions.

scholarly journals Camel Milk Mitigates Cyclosporine-Induced Renal Damage in Rats: Targeting p38/ERK/JNK MAPKs, NF-κB, and Matrix Metalloproteinases

Biology ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 442
Author(s):  
Hany H. Arab ◽  
Ahmed M. Ashour ◽  
Abdulmalik M. Alqarni ◽  
El-Shaimaa A. Arafa ◽  
Ahmed M. Kabel
Keyword(s):  
Matrix Metalloproteinases ◽  
Inflammatory Cytokines ◽  
Renal Damage ◽  
Mapk Pathway ◽  
Antioxidant Properties ◽  
Kidney Tissue ◽  
Camel Milk ◽  
Renal Inflammation ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Renal damage is a devastating adverse effect for cyclosporine; a widely used immunosuppressant drug. The present work examined the potential of camel milk, a natural agent with marked anti-inflammatory/antioxidant properties, to attenuate cyclosporine-induced renal injury. The kidney tissue was examined with the aid of Western blotting, immunohistochemistry, biochemical assays, including colorimetric and ELISA kits. The present findings revealed that camel milk (10 mL/kg/day; for 3 weeks by gavage) significantly lowered serum creatinine, BUN, and KIM-1 renal dysfunction markers. Mechanistically, camel milk inhibited renal inflammation, as seen by significant decrease of the pro-inflammatory cytokines (MCP-1, TNF-α, IL-1β, and IL-18) and extracellular degradation signals (MMP-2 and MMP-9) and enhanced the generation of the anti-inflammatory IL-10. Moreover, it inhibited the upstream pro-inflammatory p38/ERK/JNK MAPK pathway by lowering the phosphorylation of the 3 subfamilies of MAPKs (p38 MAPK, JNK1/2, and ERK1/2). Furthermore, camel milk curbed the NF-κB pathway activation by downregulating the protein expression of activated NF-κBp65, p-NF-κBp65, and p-IκBα proteins. Additionally, camel milk inhibited renal oxidative stress by lowering the MPO activity and augmenting the reduced/oxidized glutathione ratio and total antioxidant capacity. These findings propose that camel milk may be a promising agent that inhibits cyclosporine-triggered renal inflammation via curtailing the p38/ERK/JNK MAPK and NF-κB pathways, matrix metalloproteinases, and pro-inflammatory cytokines.

scholarly journals Sustained Hypoxia Suppresses Joint Destruction in a Rat Model of Rheumatoid Arthritis via Negative Feedback of Hypoxia Inducible Factor-1α

2021 ◽  
Vol 22 (8) ◽  
pp. 3898
Author(s):  
Kenta Kaihara ◽  
Shuji Nakagawa ◽  
Yuji Arai ◽  
Hiroaki Inoue ◽  
Shinji Tsuchida ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Inflammatory Cytokines ◽  
Joint Destruction ◽  
Hypoxia Inducible Factor ◽  
Inhibitory Effect ◽  
Dependent Manner ◽  
Collagen Induced Arthritis ◽  
Risk Patients ◽  
Sustained Hypoxia ◽  
Pro Inflammatory Cytokines

Hypoxia inducible factor (HIF)-1α has been implicated in the pathogenesis of rheumatoid arthritis (RA). HIF-1α, which is expressed in hypoxia, is reversely suppressed in sustained hypoxia. Here, we investigated the inhibitory effect of hypoxia on arthritis by controlling HIF-1α. Rheumatoid fibroblast-like synoviocyte MH7A cells were cultured in a hypoxic incubator for up to 72 h to evaluate the expression of HIF-1. Furthermore, collagen-induced arthritis (CIA) model rats were maintained under 12% hypoxia in a hypoxic chamber for 28 days to evaluate the effect on arthritis. In MH7A cells, HIF-1α protein level increased at 3 h, peaked at 6 h, and subsequently decreased in a time-dependent manner. The transcription of pro-inflammatory cytokines increased at 1 h; however, they decreased after 3 h (p < 0.05). Deferoxamine-mediated activation of HIF-1α abolished the inhibitory effect of sustained hypoxia on pro-inflammatory cytokines. In the rat CIA model, the onset of joint swelling was delayed and arthritis was suppressed in the hypoxia group compared with the normoxia group (p < 0.05). Histologically, joint destruction was suppressed primarily in the cartilage. Thus, sustained hypoxia may represent a new safe, and potent therapeutic approach for high-risk patients with RA by suppressing HIF-1α expression.

Sign in / Sign up

Export Citation Format

Share Document