Carboxymethyl-chitosan protects rabbit chondrocytes from interleukin-1beta-induced apoptosis.

نویسندگان

  • Qing Chen
  • Shi-Qing Liu
  • Yu-Ming Du
  • Hao Peng
  • Li-Ping Sun
چکیده

Chondrocyte apoptosis is important in pathogenesis of osteoarthritis. Chitosan is a non-toxic, biodegradable and biocompatible glycosaminoglycan. In this study, the effects of carboxymethyl-chitosan (CM-chitosan), a soluble derivative of chitosan, on chondrocyte apoptosis were investigated. Primary rabbit chondrocytes were cultured and induced to apoptosis by 10 ng/ml interleukin-1beta (IL-1beta). After treatment with various concentrations of CM-chitosan (50, 100, 200 microg/ml), the apoptotic rate, mitochondrial function, nitric oxide production, and the levels of inducible nitric oxide synthase (iNOS) mRNA and reactive oxygen species in IL-1beta-induced chondrocytes were examined. The results showed that CM-chitosan could inhibit chondrocyte apoptosis in a dose-dependent manner. Furthermore, it could partly restore the levels of mitochondrial membrane potential and ATP, decrease nitric oxide production by down-regulation of iNOS mRNA expression, and scavenge reactive oxygen species in chondrocytes induced by IL-1beta. The results suggested that the inhibitory effects of CM-chitosan on IL-1beta-induced chondrocyte apoptosis were possibly due to the protection of mitochondrial function, the decline in the levels of nitric oxide and reactive oxygen species.

برای دانلود رایگان متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Controlled Release of Interleukin-1 Receptor Antagonist from Hyaluronic Acid-Chitosan Microspheres Attenuates Interleukin-1β-Induced Inflammation and Apoptosis in Chondrocytes

This paper investigates the protective effect of interleukin-1 receptor antagonist (IL-1Ra) released from hyaluronic acid chitosan (HA-CS) microspheres in a controlled manner on IL-1β-induced inflammation and apoptosis in chondrocytes. The IL-1Ra release kinetics was characterized by an initial burst release, which was reduced to a linear release over eight days. Chondrocytes were stimulated wi...

متن کامل

Shikonin protects chondrocytes from interleukin-1beta-induced apoptosis by regulating PI3K/Akt signaling pathway.

Chondrocyte apoptosis is mostly responsible for the development and progression of osteoarthritis. IL-1β is generally served as an agent that induces chondrocyte apoptosis. Shikonin exerts its anti-inflammatory effect on cartilage protection in vivo. We aimed to explore the protective effect of shikonin on interleukin-1beta (IL-1β)-induced chondrocyte apoptosis and the potential molecular mecha...

متن کامل

Posttranscriptional effect of insulin-like growth factor-I on interleukin-1beta-induced type II-secreted phospholipase A2 gene expression in rabbit articular chondrocytes.

Large amounts of type II-secreted phospholipase A2 (type II sPLA2) are secreted into inflammatory synovial fluid and they are believed to induce the synthesis of lipid mediators by articular chondrocytes. Preliminary experiments showed that insulin-like growth factor-I, which counteracts cartilage degradation in arthritis, inhibits interleukin-1beta-induced type II sPLA2 gene expression in rabb...

متن کامل

Inhibition of interleukin-1beta-stimulated dedifferentiation of chondrocytes via controlled release of CrmA from hyaluronic acid-chitosan microspheres

BACKGROUND The previous studies indicated that CrmA could ameliorate the interleukin-1β induced osteoarthritis. In this study, we investigated the controlled-released cytokine response modifier A (CrmA) from hyaluronic acid (HA)-chitosan (CS) microspheres to improve interleukin-1β (IL-1β)-stimulated dedifferentiation of chondrocytes. METHODS A rat model of osteoarthritis (OA) in vitro was est...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

عنوان ژورنال:
  • European journal of pharmacology

دوره 541 1-2  شماره 

صفحات  -

تاریخ انتشار 2006