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01 June 2012

Selective COX-2 inhibitor ameliorates osteoarthritis by repressing apoptosis of chondrocyte

Yunsheng OuABCDEFG, Chao TanF, Hong AnA, Dianming JiangG, Zhengxue QuanD, Ke TangB, Xiaoji LuoC

DOI: 10.12659/MSM.882901

Med Sci Monit 2012; 18(6): BR247-252

Abstract

Background: Celecoxib has a positive effect on human osteoarthritic cartilage, but the mechanisms remain unclear. The aim of this study was to test whether celecoxib could inhibit the apoptosis of chondrocyte and ameliorate type II collagen synthesis to relieve symptoms of OA (osteoarthritis).
Material/Methods: 130 Wistar rats were randomly divided into 4 groups as celecoxib (CE), ibuprofen (IBP), indomethacin (IN) and normal saline group (NS). The osteoarthritis was induced by the excision of the left Achilles tendon. At the 3th, 6th, 9th month of treatment, the histological structure of articular cartilage was observed using HE staining. Type II collagen was examined using immunohistochemistry. Chondrocyte apoptosis was detected by TUNEL staining, and the change of ultra-microstructure of chondrocyte was examined through a transmission electron microscope.
Results: CE reduced the OA-like histological changes and suppressed chondrocyte apoptosis. However, IN or IBP had deleterious effects on articular cartilage and enhanced the chondrocyte apoptosis. IBP promoted the expression of type II collagen, and IN inhibited its expression, but had no effect in the CE group.
Conclusions: CE had favorable action on OA progression, and may be the ideal choice in the treatment of chronic destructive joint disease where anti-inflammatory drugs need to be used for a prolonged period.

Keywords: Osteoarthritis - pathology, Indomethacin - therapeutic use, Ibuprofen - therapeutic use, Cyclooxygenase 2 Inhibitors - therapeutic use, Collagen Type II - metabolism, Chondrocytes - ultrastructure, Cartilage, Articular - pathology, Pyrazoles - therapeutic use, Rats, Wistar, Sulfonamides - therapeutic use

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Medical Science Monitor Basic Research eISSN: 2325-4416
Medical Science Monitor Basic Research eISSN: 2325-4416