Feng Zhi-yun, He Zhen-nian, Zhang Bin, Li Yi-qiao, Guo Jian, Xu Yuan-lin, Han Ming-yuan, Chen Zhong
Spine Lab, Department of Orthopedic Surgery, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, People's Republic of China, 310003.
Department of Orthopedics, Beilun People's Hospital, No. 1288, Lu shan Road, Ningbo, Zhejiang Province, People's Republic of China, 315806.
Cell Tissue Res. 2015 Oct;362(1):187-99. doi: 10.1007/s00441-015-2194-8. Epub 2015 May 19.
Our aim is to elucidate the effects of osteoproteogerin (OPG) on cartilage destruction in rats as a model of collagen-induced arthritis (CIA). To establish the CIA model, Sprague Dawley rats were injected with bovine type II collagen solution subcutaneously via the tails. Adenovirus-mediated OPG (Ad-OPG) was then injected intra-articularly either at the beginning of CIA (early OPG treatment) or one week after CIA establishment (late OPG treatment); vehicle or Ad-green fluorescent protein were injected as controls. The rats were killed 4 weeks after treatment. Ankle-joint sections were obtained for histology. Serum samples were collected for enzyme-linked immunosorbent assay. Safranin O staining showed that proteoglycan loss was inhibited in the early and late Ad-OPG groups. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling staining revealed that both early and late Ad-OPG treatments significantly prevented chondrocyte apoptosis in CIA rats. Furthermore, disintegrin and metalloproteinase with thrombospondin motif-5 expression decreased remarkably in the early and late OPG treatment groups. However, the cartilage destruction score, cartilage oligomeric matrix protein level and caspase-3 expression were only decreased in the early Ad-OPG treatment group. Additionally, ankle-joint swelling and the interleukin-1β expression level in CIA rats were not notably altered by Ad-OPG treatment. Taken together, our results suggest that early Ad-OPG treatment has potent protective effects against cartilage destruction during rheumatoid arthritis progression, mainly by reducing proteoglycan loss and chondrocyte apoptosis.
我们的目的是阐明骨保护素(OPG)对作为胶原诱导性关节炎(CIA)模型的大鼠软骨破坏的影响。为建立CIA模型,将Sprague Dawley大鼠通过尾部皮下注射牛II型胶原溶液。然后在CIA开始时(早期OPG治疗)或CIA建立后一周(晚期OPG治疗)关节内注射腺病毒介导的OPG(Ad-OPG);注射载体或Ad-绿色荧光蛋白作为对照。治疗4周后处死大鼠。获取踝关节切片用于组织学检查。收集血清样本用于酶联免疫吸附测定。番红O染色显示,早期和晚期Ad-OPG组的蛋白聚糖损失受到抑制。末端脱氧核苷酸转移酶介导的dUTP缺口末端标记染色显示,早期和晚期Ad-OPG治疗均显著预防了CIA大鼠软骨细胞凋亡。此外,早期和晚期OPG治疗组中含血小板反应蛋白基序的解聚素和金属蛋白酶-5表达显著降低。然而,仅早期Ad-OPG治疗组的软骨破坏评分、软骨寡聚基质蛋白水平和半胱天冬酶-3表达降低。此外,Ad-OPG治疗未显著改变CIA大鼠的踝关节肿胀和白细胞介素-1β表达水平。综上所述,我们的结果表明,早期Ad-OPG治疗对类风湿性关节炎进展过程中的软骨破坏具有强大的保护作用,主要是通过减少蛋白聚糖损失和软骨细胞凋亡来实现的。