Hashemi Seyed Ali, Azad Ali, Erfani Amirhossein, Shahriarirad Reza, Azarpira Negar
Research Center for Bone and Joint Diseases, Department of Orthopedic Surgery, Chamran Hospital, Shiraz University of Medical Sciences, Shiraz, Iran.
Student Research Committee, Shiraz University of Medical Sciences, Shiraz, Iran.
J Exp Orthop. 2022 Jul 28;9(1):72. doi: 10.1186/s40634-022-00516-5.
Several cytokines and growth factors start and progress the destruction process of joint hyaline cartilage and fibrosis formation. Captopril is classified as an Angiotensin-converting enzyme inhibitor in which several studies revealed that captopril significantly decreases fibrosis formation in some organs like the liver, heart, and kidney. This study aimed to evaluate the use of captopril in reducing the possibility of arthrofibrosis and osteoarthritis in an animal model.
In this in-vivo animal model study, the anterior cruciate ligament of 24 rabbits was transected to induce osteoarthritis and arthrofibrosis. The control group contained 11 rabbits and the second group consisted of 13 rabbits. The second group was treated with 10 mg/ kilogram/day captopril through a nasogastric tube. The control group was treated with normal saline in the same way. Cartilage damage and osteoarthritis were evaluated by Osteoarthritis Research Society International (OARSI) scoring system. After 30 days, animals were sacrificed, and arthrofibrosis and cartilage damage were evaluated microscopically and macroscopically.
According to macroscopic and microscopic evaluation, captopril dramatically reduced arthrofibrosis formation based on visual scoring and the Masson trichrome staining system. Cartilage damage was lower in the intervention group compared to the control group.
Captopril is an angiotensin-converting enzyme inhibitor that demonstrated to significantly decreases the possibility of arthrofibrosis. Although the beneficial preventive effect of captopril on osteoarthritis was not proved statistically, better results may be obtained if the route of administration or drug dosage is changed.
多种细胞因子和生长因子启动并推进关节透明软骨的破坏过程及纤维化形成。卡托普利属于血管紧张素转换酶抑制剂,多项研究表明,卡托普利能显著减少肝脏、心脏和肾脏等某些器官的纤维化形成。本研究旨在评估卡托普利在动物模型中降低关节纤维化和骨关节炎发生可能性的作用。
在这项体内动物模型研究中,切断24只兔子的前交叉韧带以诱导骨关节炎和关节纤维化。对照组有11只兔子,第二组有13只兔子。第二组通过鼻胃管给予10毫克/千克/天的卡托普利。对照组以同样方式给予生理盐水。采用国际骨关节炎研究学会(OARSI)评分系统评估软骨损伤和骨关节炎情况。30天后,处死动物,通过显微镜和肉眼评估关节纤维化和软骨损伤情况。
根据宏观和微观评估,基于视觉评分和马松三色染色系统,卡托普利显著减少了关节纤维化的形成。干预组的软骨损伤低于对照组。
卡托普利是一种血管紧张素转换酶抑制剂,已证明其能显著降低关节纤维化的可能性。尽管卡托普利对骨关节炎的有益预防作用未得到统计学证实,但改变给药途径或药物剂量可能会获得更好的结果。