创伤后骨关节病手术模型动物软骨和骨组织的自由基氧化和代谢过程

S. Belova, R. Zubavlenko, E. V. Gladkova, I. Babushkina, V. Ul'yanov
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引用次数: 0

摘要

导语:创伤后骨关节病(PTOA)是由关节结缔组织成分损伤引起的,伴随着自由基的形成,激活软骨和骨吸收,导致关节组织细胞外基质生物聚合物的断裂。目的:研究膝关节上睑下垂手术模型动物软骨和骨组织自由基氧化和代谢过程的特点。材料与方法:选用大鼠31只,其中完整动物11只,pta模型动物20只。结缔组织的代谢过程通过软骨(透明质酸、聚集蛋白)和骨(成纤维细胞生长因子-23、骨保护素、硬化蛋白、骨钙素)组织生物标志物含量的变化来评估。以脂质氢过氧化物水平评价自由基氧化过程的条件,以总抗氧化剂和硫醇状态参数评价抗氧化系统的活性。结果:在PTOA模型的大鼠中,与对照组的完整动物相比,软骨组织生物聚合物聚集蛋白和透明质酸增加(p 0.001),骨形成标记物(骨钙素含量增加的趋势)和骨稳态调节标记物(成纤维细胞生长因子-23增加,p 0.001)的负变化,骨保护素和硬化蛋白含量减少的趋势。与此同时,全身血液中脂质氢过氧化物增加(p 0.01),硫醇状态指数下降(p 0.01),总抗氧化活性保持正常(p 0.05)。结论:本研究的数据表明,在手术模型的动物膝关节上睑胬肉中,骨和软骨组织中自由基氧化增强,代谢过程紊乱。骨组织代谢的负变化表现为重塑过程平衡的丧失,软骨组织的代谢紊乱表现为在自由基氧化过程加剧和硫醇系统相对紧张的情况下破坏其生物聚合物,而总抗氧化活性保持在生理规范内。从使用所研究的生物标志物来识别膝关节上睑下垂的致病诱因和确定治疗措施方向的角度来看,已确定的事实是有希望的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Free Radical Oxidation and Metabolic Processes of Cartilage and Bone Tissues in Animals with Surgical Model of Posttraumatic Osteoarthrosis
INTRODUCTION: Posttraumatic osteoarthrosis (PTOA) resulting from injuries of connective-tissue components of the joint, is accompanied by formation of free radicals activating chondro- and osteoresorption, which leads to fragmentation of biopolymers of the extracellular matrix of the joint tissues. AIM: To study the peculiarities of free radical oxidation and metabolic processes of cartilage and bone tissues in animals with a surgical model of PTOA of the knee joint. MATERIALS AND METHODS: The study was conducted on 31 rats (11 intact animals and 20 animals with PTOA model). The metabolic processes of the connective tissue were evaluated by the changes in the content of biomarkers of the cartilage (hyaluronan, aggrecan) and bone (fibroblast growth factor-23, osteprotegerin, sclerostin, osteocalcin) tissues. The condition of the free radical oxidation processes was evaluated by the level of lipid hydroperoxides, and the activity of antioxidant system by the parameters of the total antioxidant and thiol statuses. RESULTS: In rats with the PTOA model, an increase in cartilage tissue biopolymers aggrecan and hyaluronan (p 0.001) was noted with a negative change in the marker of bone formation (a tendency to increase in the content of osteocalcin) and markers of regulation of bone homeostasis (increased fibroblast growth factor-23, p 0.001), with a tendency to decrease in the content of osteoprotegerin and sclerostin, in comparison with intact animals of the control group. In parallel with this, an increase in lipid hydroperoxides (p 0.01) in the systemic bloodstream was detected with a decrease in the thiol status index (p 0.01) with preserved normal total antioxidant activity (p 0.05). CONCLUSION: The data of the conducted study evidences intensification of free radical oxidation and derangement of metabolic processes in the bone and cartilage tissues in animals with a surgical model of PTOA of the knee joint. A negative change in the metabolism of the bone tissue was manifested by the loss of balance of remodeling processes, and metabolic disorders in the cartilage tissue consisted in the destruction of its biopolymers in conditions of intensification of free radical oxidation processes and relative tension of the thiol system with the total antioxidant activity remaining within the physiological norm. The established facts are promising from the point of view of using the studied biomarkers both for the identification of pathogenetic triggers of PTOA of the knee joint, and for the determination of the direction of therapeutic measures.
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