ArticleExperimental and therapeutic medicine2017
Carboxymethyl-chitosan attenuates inducible nitric oxide synthase and promotes interleukin-10 production in rat chondrocytes.
Article in Experimental and therapeutic medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 23 citations in OpenAlex.
- Nanoceria Coated with Maltodextrin or Chitosan: Effects on Key Genes of Oxidative Metabolism, Proliferation, and Autophagy in Human Embryonic Lung Fibroblasts.Molecules (Basel, Switzerland) · 2025Article
- Therapeutic mechanisms of polysaccharides in the management of rheumatoid arthritis: a comprehensive review.Frontiers in immunology · 2025Review
- Yangyin Huowei mixture alleviates chronic atrophic gastritis by inhibiting the IL-10/JAK1/STAT3 pathway.World journal of gastrointestinal surgery · 2024Article
- The Role of Regulated Programmed Cell Death in Osteoarthritis: From Pathogenesis to Therapy.International journal of molecular sciences · 2023Review
- The potential roles of JAK/STAT signaling in the progression of osteoarthritis.Frontiers in endocrinology · 2022Review
- Health concerns of lambs fed cottonseed hulls combined with chitosan by examining the blood metabolic profile and histopathology of the kidney, liver, and rumen.Veterinarni medicina · 2021Article
- From Pathogenesis to Therapy in Knee Osteoarthritis: Bench-to-Bedside.International journal of molecular sciences · 2021Review
- Expression of Nitric Oxide Synthase and Nitric Oxide Levels in Peripheral Blood Cells and Oxidized Low-Density Lipoprotein Levels in Saliva as Early Markers of Severe Dengue.BioMed research international · 2021Article
- Mitochondrial dependent pathway is involved in the protective effects of carboxymethylated chitosan on nitric oxide-induced apoptosis in chondrocytes.BMC complementary medicine and therapies · 2020Article
- RNA Sequencing Reveals LINC00167 as a Potential Diagnosis Biomarker for Primary Osteoarthritis: A Multi-Stage Study.Frontiers in genetics · 2020Article
- Chitosans for Tissue Repair and Organ Three-Dimensional (3D) Bioprinting.Micromachines · 2019Review
- Progress in the Development of Chitosan-Based Biomaterials for Tissue Engineering and Regenerative Medicine.Biomolecules · 2019Review
- Article
- Protective Effect of Methane-Rich Saline on Acetic Acid-Induced Ulcerative Colitis via Blocking the TLR4/NF-Oxidative medicine and cellular longevity · 2019Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Osteoarthritis (OA) is a common age-related degenerative joint disease, which is caused by the breakdown of joint cartilage and the underlying bone. Carboxymethyl (CM)-chitosan is a soluble derivative of chitosan that has similar physicochemical properties to the extracellular proteoglycans identified in hyaline cartilage. Previous studies have demonstrated that CM-chitosan serves a protective role in a rabbit OA model. The aim of the present study was to investigate the effect of CM-chitosan on NO production and inflammation through its upregulation of interleukin (IL)-10, and the activation of the janus kinase (JAK)/signal transducer and activator of transcription (STAT)/suppressor of cytokine signaling (SOCS) signaling pathway. In the present study primary rat chondrocytes were induced to inflammation with 2 µg/ml lipopolysaccharide. The cells were subsequently subjected to increasing concentrations of CM-chitosan (50, 100 and 200 µg/ml) and the relative mRNA and protein expression of inducible nitric oxide synthase (iNOS), IL-10, JAK1, STAT3 and SOCS3 were measured by RT-qPCR and western blot analysis respectively. The results revealed that CM-chitosan attenuated inflammation by significantly reducing iNOS expression and upregulating the anti-inflammatory cytokine IL-10 in a dose-dependent manner (P<0.05). The expression of JAK1, STAT3 and SOCS3 were also significantly upregulated by CM-chitosan (all P<0.05). The protective role of CM-chitosan against NO production was due to its upregulation of IL-10 and its activation of the JAK/STAT/SOCS signaling pathway.
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