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萘普生治疗可抑制骨关节炎大鼠模型的关节软骨丢失。

Naproxen treatment inhibits articular cartilage loss in a rat model of osteoarthritis.

机构信息

Department of Orthopaedics, Rutgers-New Jersey Medical School, Newark, New Jersey, USA.

Rutgers-School of Graduate Studies, Newark Health Sciences Campus, Newark, New Jersey, USA.

出版信息

J Orthop Res. 2021 Oct;39(10):2252-2259. doi: 10.1002/jor.24937. Epub 2020 Dec 15.

Abstract

The effects of naproxen, a nonsteroidal anti-inflammatory drug (NSAID), on articular cartilage degeneration in female Sprague-Dawley rats was examined. Osteoarthritis (OA) was induced by destabilization of the medial meniscus (DMM) in each knee. Rats were treated with acetaminophen (60 mg/kg), naproxen (8 mg/kg), or 1% carboxymethylcellulose (placebo) by oral gavage twice daily for 3 weeks, beginning 2 weeks after surgery. OA severity was assessed by histological Osteoarthritis Research Society International (OARSI) scoring and by measuring proximal tibia cartilage depth using contrast enhanced µCT (n = 6 per group) in specimens collected at 2, 5, and 7 weeks after surgery as well as on pristine knees. Medial cartilage OARSI scores from the DMM knees of naproxen-treated rats were statistically lower (i.e., better) than the medial cartilage OARSI scores from the DMM knees of placebo-treated rats at 5-weeks (8.7 ± 3.6 vs. 13.2 ± 2.4, p = 0.025) and 7-weeks (9.5 ± 1.2 vs. 12.5 ± 2.5, p = 0.024) after surgery. At 5 weeks after DMM surgery, medial articular cartilage depth in the proximal tibia specimens was significantly greater in the naproxen (1.78 ± 0.26 mm, p = 0.005) and acetaminophen (1.94 ± 0.12 mm, p < 0.001) treated rats as compared with placebo-treated rats (1.34 ± 0.24 mm). However, at 7 weeks (2 weeks after drug withdrawal), medial articular cartilage depth for acetaminophen-treated rats (1.36 ± 0.29 mm) was significantly reduced compared with specimens from the naproxen-treated rats (1.88 ± 0.14 mm; p = 0.004). The results indicate that naproxen treatment reduced articular cartilage degradation in the rat DMM model during and after naproxen treatment.

摘要

考察了非甾体抗炎药(NSAID)萘普生对雌性 Sprague-Dawley 大鼠关节软骨退化的影响。通过内侧半月板(DMM)不稳定在每个膝关节中诱导骨关节炎(OA)。术后 2 周,通过口服灌胃每天两次给予乙酰氨基酚(60mg/kg)、萘普生(8mg/kg)或 1%羧甲基纤维素(安慰剂)治疗 3 周。在手术 2、5 和 7 周后以及在原始膝关节处采集标本,通过组织学骨关节炎研究协会国际(OARSI)评分和使用对比增强μCT 测量近端胫骨软骨深度(每组 n=6)评估 OA 严重程度。与安慰剂治疗的 DMM 膝关节相比,萘普生治疗的大鼠的内侧软骨 OARSI 评分在 5 周(8.7±3.6 对 13.2±2.4,p=0.025)和 7 周(9.5±1.2 对 12.5±2.5,p=0.024)时统计学上更低(即更好)。在 DMM 手术后 5 周,与安慰剂治疗的大鼠相比,萘普生(1.78±0.26mm,p=0.005)和乙酰氨基酚(1.94±0.12mm,p<0.001)治疗的大鼠的近端胫骨标本中的内侧关节软骨深度显着更大。然而,在 7 周(药物停药后 2 周)时,与萘普生治疗的大鼠相比,乙酰氨基酚治疗的大鼠的内侧关节软骨深度(1.36±0.29mm)显着降低(p=0.004)。结果表明,在萘普生治疗期间和之后,萘普生治疗可减少大鼠 DMM 模型中的关节软骨降解。

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