Melatonin Attenuates the Progression of Osteoarthritis in Rats by Inhibiting Inflammation and Related Oxidative Stress on the Surface of Knee Cartilage. Issue 9 (27th July 2022)

• Record Type: Journal Article
• Authors: Ke, Chenghui; Li, Hongyun; Yang, Dan; Ying, Hao; Zhu, Hongwen; Wang, Jian; Xu, Jun; Wang, Lin
• Is Part Of: Orthopaedic surgery. Volume 14:Issue 9(2022)
• Page Start: 2230
• Page End: 2237
• Publication Date: 2022-07-27
• Subjects: Inflammatory factor -- Melatonin antagonist -- Osteoarthritis model -- Papain -- SD male rats; Orthopedic surgery -- Periodicals; Orthopedics -- Periodicals; Musculoskeletal system -- Wounds and injuries -- Periodicals; 617.47005
• DOI: 10.1111/os.13408
• Languages: English
• ISSNs: 1757-7853

Abstract

Abstract : Objective: To investigate the correlation between melatonin and osteoarthritis (OA) in rats. To explore the relevant mechanisms in the occurrence and development of osteoarthritis in rats, and to further understand the disease of osteoarthritis. Methods: Forty healthy 6‐month‐old male SD rats were randomly divided into two groups: sham and drug intervention groups. Pre‐OA modeling, enzyme‐linked immunosorbent assay was employed to detect the levels of IL‐1β, IL‐6, COX‐2, and melatonin in the serum of the rats in each group. For OA modeling, we administered an injection of papain into the knee cavity of all rats. The levels of IL‐1β, IL‐6, and COX‐2 in the serum of rats in each group were detected 2 weeks after the modeling. Additionally, 2 weeks after the modeling, the rats in the drug intervention group were intraperitoneally injected with melatonin antagonists. The rats in the sham group were intraperitoneally injected with normal saline for 2 weeks. The levels of IL‐1β, IL‐6, and COX‐2 in the serum of each group were measured at the second, third, and fourth weeks after the drug intervention, and the levels of melatonin in the serum were measured at the second week after the drug intervention. Finally, the rats were euthanized by cervical dislocation, and pathological sections were collected from the knee joint to observe the pathological tissue changes under a microscope, and Mankin score was determined. The independent samples t ‐test method was used for analysis. Results: The imaging examination after the drug intervention showed that the modeling of knee osteoarthritis in rats was successful. In the pathological findings, HE staining showed a legible cartilage structure of each layer, with cartilage proliferation and partial cartilage tearing to the radial layer. The tide line was intact; toluidine blue staining revealed more obvious changes. The differences among the mean values of IL‐6, IL‐1β, and COX‐2 measured in each period were statistically significant ( t = 5.50, p < 0.05). The measured mean values of IL‐6, IL‐1β, and COX‐2 revealed statistically significant differences among the groups ( t = 2.01, p < 0.05). The intergroup comparison of the Mankin scores in each period showed statistically significant differences. Conclusion: Melatonin may inhibit inflammation and associated oxidative stress on the surface of knee cartilage. It may be related to the repair and regeneration of articular surface cartilage during the development of OA in the rat knee joint. Abstract : In this experiment, after the above three pro‐inflammatory factors were modeled in osteoarthritis (OA), their blood content levels gradually increased with the progress of the experiment, and they were statistically significant, indicating that in the case of melatonin reduction, each of the index increased significantly, indicating that the mechanism of melatonin in the repair and regeneration of cartilage on the knee joint may be caused by inhibiting inflammation and related oxidative stress on the surface of knee cartilage. We preliminarily explored the correlation between melatonin and OA, and even the correlation between melatonin and IL‐1β, IL‐6 and COX‐2, and clarified the effect of melatonin on OA mechanism. However, there are still some shortcomings in this experiment, and the correlation between melatonin and OA at the molecular level or even the gene level needs to be further explored to provide a basis for clinical prevention and treatment of OA.