Carboxymethyl-chitosan protects rabbit chondrocytes from interleukin-1beta-induced apoptosis.
نویسندگان
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.
منابع مشابه
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متن کاملAuthor's response to reviews Title:Inhibition of Interleukin-1beta-Stimulated Dedifferentiation of Chondrocytes via Controlled Release of CrmA from hyaluronic acid-Chitosan Microspheres
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متن کاملInhibition 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...
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عنوان ژورنال:
- European journal of pharmacology
دوره 541 1-2 شماره
صفحات -
تاریخ انتشار 2006