摘要
目的探讨美洛昔康在慢性肩袖损伤防治中的作用机制。方法将36只大鼠用计算机随机数字生成软件随机分为模型组,美洛昔康组,正常对照组,每组12只。模型组和美洛昔康组双侧肩关节行慢性肩袖损伤造模手术,正常对照组不做处理。各组大鼠均于术后第4天开始跑台运动(下倾13.5°、17 m/min),每天1次,每次30 min。美洛昔康组于术后第3周、第4周、第5周各进行1次美洛昔康肩峰下注射操作,每次0.3 ml,浓度为3 mg/ml。模型组和正常对照组于相同时间注射等量生理盐水。3组大鼠于术后6周处死,取双侧肩关节标本:每只大鼠均选取一侧肩关节标本做石蜡包埋,HE、Masson、PGE2免疫组化染色;另一侧肩关节解剖出冈下肌-肱骨标本,做生物力学拉断测试,并提取肌腱总蛋白,Western-blot检测BMP-2表达水平。结果 HE及Masson染色可见模型组胶原纤维排列松散,纤维束分层,肌腱近止点处胶原连续性中断;正常对照组肌腱胶原平行、紧密;美洛昔康组胶原连续但排列疏松。模型组与美洛昔康组和正常对照组比较,PGE2表达明显增高,差异均有统计学意义(P<0.001)。美洛昔康组与正常对照组比较,PGE2表达差异无统计学意义(P=0.4246)。生物力学试验示冈下肌腱最大负荷,美洛昔康组(38.95±8.397)N低于正常对照组(71.66±5.3312)N,差异有统计学意义(P<0.001);模型组(17.95±6.689)N显著低于美洛昔康组(P<0.001)和正常对照组(P<0.001),差异均有统计学意义。肌腱组织BMP-2相对表达量,模型组(2.0230±0.2042)较美洛昔康组(0.4508±0.1274)和正常对照组(0.1458±0.0613)显著升高,差异均有统计学意义(P<0.001);结论 PGE2高表达促使肌腱干细胞自分泌骨形态发生蛋白-2是导致慢性肩袖损伤的原因之一。美洛昔康通过抑制PGE2对慢性肩袖损伤具有一定预防或治疗效果。
Objective To investigate the mechanism of meloxicam in preventing chronic rotator cuff injury. Methods A total of 36 rats were randomly and evenly divided into the model group, meloxicam group and normal control group （ n = 12 ）. Model group and meloxicam group received bilateral modeling surgery, while the normal control group not. All rats were exposed to 30 minutes of downhill running at the speed of 17 m / min （ -13.5＆#176; ） every day at the fourth day after the operation. Meloxicam group received meloxicam （ concentration of 3 mg / ml ） subacromial injection at the third week, the fourth week and the fifth week after the modeling, 0.3 ml each time. Model group and the normal control group were injected with 0.3 ml saline at the same time. All rats were sacrificed at the sixth week and bilateral shoulder specimens were collected. For each rat, one shoulder was randomly selected to receive HE, Masson and PGE2 immunohistochemical staining. The other shoulder was used to detect BMP-2 expression level with Western-blot technology after the biomechanical testing. Results HE and Masson staining： each group showed no inflammatory cell infiltration; full-thickness tear could be found in all cases in the model group, with severe fiber layering; partial tendon tear and lighter collagen layering could be observed in the meloxicam group; infraspinatustendon in the normal control group was smooth and continuous, no obvious abnormalities. The expressions of PGE2 in the model group were significantly higher than those in both the meloxicam group and the normal control group （ P 〈 0.001 ）. Meloxicam group was compared with the control group, PGE2 showed no statistically significant difference （ P = 0.4246 ）. The maximal loadings of tendons in the model group （ 17.95 ± 6.689 ） N were significantly lower than those in both the meloxicam group （ 38.95 ± 8.397 ） N and the normal control group （ 71.66 ± 5.3312 ） N （ P 〈 0.001 ）. The maximal loadings of tendons in the meloxicam group were significantly lower than those in the normal control group （ P 〈 0.001 ）. The expressions of BMP-2 in the model group （ 2.0230 ± 0.2042 ） were significantly higher than those in both the meloxicam group （ 0.4508 ± 0.1274 ） and the normal control group （ 0.1458 ± 0.0613 ） （ P 〈 0.001 ）. The expressions of BMP-2 in the normal control group （ 0.1458 ± 0.0613 ） were significantly lower than those in the meloxicam group （ P 〈 0.001 ）. Conclusions PGE2 expression is one of the causes of chronic rotator cuff injury. Meloxicam can prevent or heal chronic rotator cuff injury to some extent by inhibiting PGE2.
作者
艾克热木江·阿尔肯
葛云林
丁舒晨
王哲洋
刘志荣
王大伟
金晓均
陈利英
AERKEN Aikeremujiang;GE Yun-lin;DING Shu-chen;WANG Zhe-yang;LIU Zhi-rong;WANG Da-wei;JIN Xiao-jun;CHEN Li-ying
出处
《中国骨与关节杂志》
CAS
2017年第12期947-953,共7页
Chinese Journal of Bone and Joint
基金
杭州市卫生计生科技计划项目(2016B62)
关键词
肩关节
前列腺素
创伤和损伤
肩袖
Shoulder joint
Prostaglandins
Wounds and injuries
Rotator cuff
