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- Title
Tumor necrosis factor alpha-stimulated gene-6 (TSG-6) inhibits the inflammatory response by inhibiting the activation of P38 and JNK signaling pathway and decreases the restenosis of vein grafts in rats.
- Authors
Zhang, Chengxin; Zhang, Biao; Wang, Huiping; Tao, Qianshan; Ge, Shenglin; Zhai, Zhimin
- Abstract
This study aims to explore the effects of tumor necrosis factor alpha-stimulated gene-6 (TSG-6) on vascular inflammatory response and vascular injury in grafted vein wall of rats and its possible mechanism. Vascular grafting model was established by modified cuff. The effect of TSG-6 on the inflammatory response and vascular injury of vein graft was investigated. The activation of mast cells and macrophages after LPS stimulation was observed by lentivirus-mediated upregulation or downregulation of TSG-6 expression. The results showed that rhTSG-6 treatment could significantly inhibit the proliferation of venous bridge, decrease macrophage infiltration and smooth muscle cell proliferation. The expression levels of TNF-α and IL-1 in treated group were significantly lower than that of untreated group ( P < 0.05), while the expression of IL-10 in treated group were significantly higher than that of untreated group ( P < 0.05). The expression levels of P38, p-P38, JNK and p-JNK in venous bridge of rats were significantly lower than those of untreated rats ( P < 0.05), while there was no significant difference in the expression level of ERK and p-ERK ( P > 0.05). TSG-6 could inhibit the proliferation of mast cells and macrophages and the release of inflammatory cytokines by down regulating the expression levels of P38, p-P38, JNK and p-JNK. TSG-6 can inhibit the inflammatory response of transplanted vein grafts in rats and reduce vascular injury by downregulation of P38 and JNK signaling pathway.
- Subjects
TUMOR necrosis factors; CORONARY artery surgery; INFLAMMATION; ENZYME inhibitors; C-Jun N-terminal kinases; CELLULAR signal transduction; CORONARY restenosis; LABORATORY rats
- Publication
Heart & Vessels, 2017, Vol 32, Issue 12, p1536
- ISSN
0910-8327
- Publication type
Article
- DOI
10.1007/s00380-017-1059-3