摘要
目的观察非甾体抗炎药对人骨关节炎(OA)软骨细胞增殖和基质代谢的影响。方法培养原代人膝OA软骨细胞,实验设立对照组、塞来昔布组、双氯芬酸组、布洛芬组。药物对细胞增殖的影响应用免疫荧光法测定5-溴脱氧尿嘧啶核苷(BrdU),酶联免疫吸附法(ELISA)检测细胞内和培养上清液中蛋白多糖(PG)、Ⅱ型胶原的含量,并比较各组间水平差异。结果布洛芬组BrdU阳性率较其他组增高(P<0.05)。双氯芬酸组软骨细胞上清液中Ⅱ型胶原含量较其他组增加(P<0.05或P<0.01);布洛芬组软骨细胞上清液中PG含量较其他组增高(P<0.05或P<0.01);诸药物组软骨细胞内Ⅱ型胶原和PG含量差异无统计学意义(P>0.05)。结论布洛芬可刺激人OA软骨细胞增殖和促进细胞分泌PG,双氯芬酸可促进人OA软骨细胞分泌Ⅱ型胶原,未观察到塞来昔布对人OA软骨细胞增殖和基质代谢存在影响。
Objective To observe the effects of nonsteroidal anti-inflammatory drugs (NSAIDs) on the proliferation of chondrocytes and metabolism of human osteoarthritis (OA) in short-term (48 hours). Methods The human knee OA chondrocytes were cultured in the presence or absence of NSAIDs (celecoxib, diclofenac and ibuprofen). BrdU assays were used to evaluate the effects of NSAIDs on the proliferation of OA chondrocytes. ELISA was used to detect the contents of proteoglycan and type- II collagen in chondrocytes and culture supernatant. The differences of those indexes were compared between groups. Results The positive rate of BrdU labelling index of chondrocytes increased significantly in ibuprofen group than that of other groups (P 〈 0.05). The content of type- II collagen in the culture supernatant increased significantly in diclofenac group than that of other groups (P 〈 0.05 or P 〈 0.01). The content of proteoglycan in the culture supernatant increased significantly in ibuprofen group than that of other groups (P 〈 0.05 or P 〈 0.01). There were no significant differences in the content of type- II collagen and proteoglycan between chondrocytes of NSAIDs groups (P 〉 0.05). Conclusion Ibu- profen may stimulate the proliferation and the secretion of proteoglycan of human OA chondrocytes. Diclofenac may stimu- late the secretion of type- II collagen of human OA chondrocytes. There were no effects of celecoxib on the proliferation and metabolism of human OA chondrocytes.
出处
《天津医药》
CAS
北大核心
2013年第9期867-870,共4页
Tianjin Medical Journal
关键词
消炎药
非甾类
骨关节炎
软骨细胞
细胞增殖
代谢
anti-inflammatory agents, non-steroidal
osteoarthritis
chondrocytes
cell proliferation
metabolism