Blockade of interleukin 6 by rat anti-mouse interleukin 6 receptor antibody promotes fracture healing
- Autores: Huang L.1, Liu S.2, Song T.3, Zhang W.3, Fan J.3, Liu Y.3
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Afiliações:
- Southern Medical University, Nanfang Hospital, Department of Burn
- Panzhihua Central Hospital, Department of Orthopaedics
- Department of Orthopaedics, Honghui Hospital
- Edição: Volume 82, Nº 10 (2017)
- Páginas: 1193-1199
- Seção: Article
- URL: https://journals.rcsi.science/0006-2979/article/view/151488
- DOI: https://doi.org/10.1134/S0006297917100121
- ID: 151488
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Resumo
Level of interleukin 6 (IL-6) is associated with fracture healing. This study was performed to explore the effect of IL-6 blockade on fracture healing. Clinical serum levels of IL-6 and tumor necrosis factor-α (TNF-α) were evaluated by enzyme-linked immunosorbent assay (ELISA). For animal experiments, the IL-6 levels after fracture and treatment with rat anti-mouse IL-6 receptor antibody (MR16-1) were assessed. Then, mice were assigned into four or seven groups: control group, fracture group, isotype IgG group, and MR16-1 groups. Serum levels of IL-6 and TNF-α, relative flexural rigidity, and mRNA levels of osteoblast-specific genes were respectively assayed by ELISA, three-point bending test, and quantitative reverse transcription PCR (qRT-PCR). Serum levels of IL-6 and TNF-α after fracture in humans and mice were increased. The increase in IL-6 and TNF-α levels in murine serum was attenuated by MR16-1 treatment. The three-point bending test showed the relative flexural rigidity of the femur was decreased after fracture, whereas the decrease was alleviated by MR16-1 treatment. The qRT-PCR results demonstrated mRNA levels of osteoblast-specific genes were upregulated after fracture and then further upregulated by MR16-1 treatment in a dose-dependent manner. Collectively, the serum level of IL-6 was elevated after fracture both in clinical and murine samples. IL-6 blockade by MR16-1 promoted fracture healing, which might be associated with changes in expression of osteoblast-specific genes.
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Sobre autores
Lei Huang
Southern Medical University, Nanfang Hospital, Department of Burn
Email: liuyang152@126.com
República Popular da China, Guangzhou, 510515, Guangdong
Shaojiang Liu
Panzhihua Central Hospital, Department of Orthopaedics
Email: liuyang152@126.com
República Popular da China, Panzhihua, 617067, Sichuan
Tao Song
Department of Orthopaedics, Honghui Hospital
Email: liuyang152@126.com
República Popular da China, Xi’an, 710054, Shaanxi
Wentao Zhang
Department of Orthopaedics, Honghui Hospital
Email: liuyang152@126.com
República Popular da China, Xi’an, 710054, Shaanxi
Jinzhu Fan
Department of Orthopaedics, Honghui Hospital
Email: liuyang152@126.com
República Popular da China, Xi’an, 710054, Shaanxi
Yang Liu
Department of Orthopaedics, Honghui Hospital
Autor responsável pela correspondência
Email: liuyang152@126.com
República Popular da China, Xi’an, 710054, Shaanxi