SummaryBackgroundCelecoxib 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/Methods130 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.ResultsCE 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.ConclusionsCE 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.
The effects of long-term use of celecoxib, ibuprofen, and indomethacin on types I, II, and III collagen metabolism were evaluated in rat osteoarthritis (OA) model. One hundred and thirty wistar rats were randomly divided into 4 groups: the celecoxib group, the ibuprofen group, the indomethacin group, and the normal saline group. The osteoarthritis was induced by the excision of the left Achilles tendon. In the 3rd, 6th, and 9th month of treatment after surgically induced osteoarthritis, the articular cartilage was observed with microscope using HE staining. The expression of proteoglycans was semiquantified using toluidine blue staining. And, the expressions of types I, II, and III collagen in chondrocytes were examined using immunohistochemistry. The results suggested that celecoxib had no remarkable effects on the expression of types I, II, and III collagen. Ibuprofen upgraded the expression of types I, II, and III collagen and increased the synthesis of collagen. Indomethacin suppressed the expression of type II collagen and enhanced the expression of types I and III collagen. Therefore, during the long-term use of NSAIDs in osteoarthritis, celecoxib may have no remarkable influences on collagen metabolism of the articular cartilage and may be the ideal choice in the treatment of chronic destructive joint disease when anti-inflammatory drugs need to be used for a prolonged period. Ibuprofen may be unfavorable, and indomethacin may be harmful to collagen metabolism in OA treatment.
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