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Blockade of Interleukin 6 by Rat Anti-mouse Interleukin 6 Receptor Antibody Promotes Fracture Healing

Lei Huang1#, Shaojiang Liu2#, Tao Song3, Wentao Zhang3, Jinzhu Fan3, and Yang Liu3*

1Southern Medical University, Nanfang Hospital, Department of Burn, Guangzhou 510515, Guangdong, China

2Panzhihua Central Hospital, Department of Orthopaedics, Panzhihua 617067, Sichuan, China

3Department of Orthopaedics, Honghui Hospital, Xi’an Jiaotong University, Xi’an 710054, Shaanxi, China; E-mail: liuyang152@126.com

# These authors contributed equally to this work.

* To whom correspondence should be addressed.

Received February 10, 2017; Revision received August 25, 2017
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.
KEY WORDS: type II procollagen, type X procollagen, receptors, interleukin 6, tumor necrosis factor-α

DOI: 10.1134/S0006297917100121