| Objective: To study the possible mechanism of swimming exercise for knee osteoarthritis by investigating the expression of swimming exercise on the expression of protein kinase R-like endoplasmic reticulum kinase (PERK) as a signaling pathway of endoplasmic reticulum stress. Methods: Sprague Dawley rats were randomly divided into a normal group (group A), sham operation group (group B), model control group (group C), and swimming exercise group (group D). Rats in group A were allowed for free activities in their cage for 8 weeks, and rats in groups B and C were allowed for free activities in their cage for 8 weeks after the sham operation and experimental operation, respectively. Rats in group D were allowed for free activities for 4 weeks after the operation and then underwent swimming exercises for 4 weeks. The cartilage changes, hematoxylin-eosin (HE) staining, toluidine blue staining, immunohistochemical staining, Mankin’s grade, gross scores, and the PERK contents in chondrocytes were compared among the groups. Results: Cartilage degradation was more severe in groups C and D than in group A as shown by gross observation, gross scores, HE staining, and toluidine blue staining (P<0.05). No significant differences were noted between groups A and B. The changes in group D were significantly less severe than those in group C (P<0.05). Immunohistochemical staining showed that the expression of PERK in articular cartilage was higher in groups C and D than in groups A and B (P<0.05), and lower in group D than in group C (P<0.05). Conclusion: Swimming exercise can promote the repair of articular cartilage possibly by reducing the expression of PERK, endoplasmic reticulum stress, and apoptosis rate of chondrocytes. |
