Abstract
Objective To observe the dynamic changes in oxidative stress and the expression levels of antioxidant and oxidative parameters in the blood and synovial fluid in the osteochondral defects of the rabbit knee joints and to explore the significance. Methods Thirty New Zealand white rabbits were randomly selected and divided into a blank control group (n = 10), a model control group (n = 10), and an osteochondral defect group (n = 10). The osteochondral defect model of rabbit knee joint was constructed by medial parapatellar arthrotomy. The expression levels of glutathione (GSH), malondialdehyde (MDA), superoxide dismutase (SOD), and 8-hydroxydeoxyguanosine (8-OHdG) in peripheral venous blood and knee synovial fluid of the three groups were measured at the end of the 4th, 8th, and 12th weeks after treatment. Results The expression levels of GSH and SOD in the blood and synovial fluid in the osteochondral defect group at the end of the 8th and 12th weeks were observably lower than those of the other two groups (P < 0.05); higher expression levels of MDA and 8-OHdG in the blood and synovial fluid of the osteochondral defect group compared with those of the other two groups were obtained (P < 0.05). At the end of the 4th, 8th, and 12th weeks, the expression levels of MDA and 8-OHdG in the blood and synovial fluid of the osteochondral defect group presented an upward trend (P < 0.05). Conclusion The osteochondral defects initiate the oxidative stress in the body, which is presented as the decrease of GSH and SOD expression, and the upregulation of MDA and 8-OHdG expression.
Highlights
Osteoarthritis (OA) is the most common joint degenerative disease in the world, to which the middle-aged and elderly population are more susceptible [1]
Compared with the blank control group, the model control group and the osteochondral defect group yielded a downward trend of the GSH and superoxide dismutase (SOD) in the blood and synovial fluid and an upward trend of the MDA and 8-OHdG at the end of the fourth week; the differences were not considered statistically significant (P > 0:05), as shown in Tables 3 and 4
Oxidative stress is involved in the pathogenesis of hypertension, atherosclerosis, diabetes, osteoporosis, and cancer
Summary
Osteoarthritis (OA) is the most common joint degenerative disease in the world, to which the middle-aged and elderly population are more susceptible [1]. Oxidative stress results from an imbalance between the oxidative and antioxidant systems of cells and tissues and is the result of excessive production of oxidative free radicals and related reactive oxygen species (ROS). A large number of studies have confirmed a close relationship of the oxidative stress triggered by the slow production of endogenous ROS to the osteochondral defects [6, 7]. Studies have shown that excessively generated free radicals give rise to osteochondrocyte apoptosis and degrade the extracellular matrix, which eventually results in osteochondral defects [8, 9]. The current research interest lies more on the relationship between oxidative stress and the process of osteochondral defects at a certain time point. This study is to preliminarily explore the relationship between osteochondral defects and oxidative stress in rabbit knee joints
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