Myrtol improves post-traumatic knee osteoarthritis by regulation of reactive oxygen species, transforming growth factor β1 and apoptosis in a mouse model

被引:13
作者
Duan, Liqun [1 ]
Zhang, Wenzhi [1 ]
Zhang, Feng [1 ]
Cai, Haiping [1 ]
机构
[1] Anhui Prov Hosp, Dept Orthoped, 17 Lujiang Rd, Hefei 230001, Anhui, Peoples R China
关键词
myrtol; post-traumatic knee osteoarthritis; reactive oxygen species; transforming growth factor-beta 1; INTRAARTICULAR FRACTURE; SYNOVIAL INFLAMMATION; CARTILAGE DAMAGE; CHONDROCYTES; INJURY; ARTHROPLASTY; TGF-BETA-1; ARTHRITIS;
D O I
10.3892/etm.2017.5367
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
100103 [病原生物学]; 100218 [急诊医学];
摘要
The present study tested whether myrtol improves post-traumatic knee osteoarthritis (PTKO) by regulating the reactive oxygen species (ROS), transforming growth factor beta 1 (TGF-beta 1) and apoptosis in a mouse model. PTKO model mice were administered with 150, 300 or 450 mg/kg myrtol for 8 weeks. ELISA analysis was used to measure tumor necrosis factor-alpha, interleukin-6, malondialdehyde, superoxide dismutase, reactive oxygen species and TGF-beta 1 levels. Caspase-3 and Bax protein expressions were analyzed using western blot analysis. In the current study, treatment with myrtol improved the tissue damage and osteoarthritis score, while it also reversed the subchondral bone thickness, subchondral bone density, trabecular bone volume/relative trabecular bone volume ratio and trabecular bone spacing in PTKO mice. The activity of tumor necrosis factor a, interleukin-6, TGF-beta 1, malondialdehyde, superoxide dismutase and ROS were effectively inhibited, and the protein expression of caspase-3 and Bax were clearly suppressed by treatment with myrtol in a mouse model of PTKO. In conclusion, the results demonstrated that myrtol treatment improved PTKO through the suppression of inflammation, oxidative stress, ROS, TGF-beta 1 and Bax/caspase-3 in mice, and myrtol may be a potential agent for clinical therapy.
引用
收藏
页码:393 / 399
页数:7
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