Chinese Journal of Tissue Engineering Research ›› 2016, Vol. 20 ›› Issue (52): 7836-7843.doi: 10.3969/j.issn.2095-4344.2016.52.012

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Ethyl linoleate inhibits inflammatory reaction induced by titanium particles and its mechanism

Liu Guo-dong1, Xin Bing2, Huang Dong2, Zheng Bai1, Sun Bai-han1, Guo Kai-jin3
  

  1. 1Graduate School of Xuzhou Medical University, Xuzhou 221004, Jiangsu Province, China; 2Department of Spine Surgery, 3Department of Joint Surgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221004, Jiangsu Province, China
  • Received:2016-09-25 Online:2016-12-16 Published:2016-12-16
  • Contact: Guo Kai-jin, Professor, Department of Spine Surgery, Affiliated Hospital of Xuzhou Medical University, Xuzhou 221004, Jiangsu Province, China
  • About author:Liu Guo-dong, Studying for master’s degree, Graduate School of Xuzhou Medical University, Xuzhou 221004, Jiangsu Province, China
  • Supported by:

    the Science Research Foundation of the Health Department, No. LW201004; the Science and Technology Project of Xuzhou, No. XM13B080

Abstract:

BACKGROUND: Ethyl linoleate has been proved to attenuate the inflammatory-cytokines release induced by lipopolysaccharide, but whether it can inhibit titanium-induced osteolysis and the underlying mechanism remain unclear.
OBJECTIVE: To observe the effect of ethyl linoleate on the expression of inflammatory-related factors induced by titanium particles and explore its mechanism.
METHODS: Forty-eight Kunming mice were randomly divided into blank control, titanium, dimethylsulfoxide (DMSO) and experimental groups. The back air pouch Inflammatory models were established in the mice of the titanium, DMSO and experimental groups, in which the 200 µL menstruum of DMSO (0.5%) and 200 µL ethyl linoleate (0.5%) were respectively administered into the pouch of the mice at 12 hours. Mice in the blank control group received no intervention. Fourteen days later, the inflammatory cell infiltration in the skin was examined through hematoxylin-eosin staining; the expression levels of inhibitor κB-α, nuclear factor-κB, inducible nitric oxide synthase, cyclooxygenase-2, tumor necrosis factor-α and interleukin-6 as well as ERK, p-ERK, JNK, p-JNK, p38 and p-p38 in MAPK signaling pathways were evaluated by western blot assay.
RESULTS AND CONCLUSION: In the titanium group and DMSO group, there were numerous inflammatory cells and vacuole-like necrotic tissues in the hair follicle lacuna of dermis and loose connective tissues of hypodermis. The experiment group showed significant reduction in inflammatory cell infiltration and vacuole-like necrosis. Compared with the blank control group, the expression levels of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κB, tumor necrosis factor-α, interleukin-6, ERK, JNK and p38 in the DMSO and titanium groups were significantly increased, while inhibitor κB-α significantly decreased (P < 0.05). Compared with the DMSO and titanium groups, there were significantly down-regulated levels of inducible nitric oxide synthase, cyclooxygenase-2, nuclear factor-κB, tumor necrosis factor-α, interleukin-6, ERK, JNK and p38, and up-regulated inhibitor κB-α level in the experimental group (P < 0.05). In conclusion, ethyl linoleate can remarkably suppress the expressions of titanium-induced inflammatory factors associated with the inhibition of nuclear factor-κB and MAPK signaling pathway activation.

Key words: Titanium, Inflammation, NF-κappa B, Tissue Engineering

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