氧化应激
肿瘤坏死因子α
污渍
NFKB1型
活力测定
下调和上调
NF-κB
p38丝裂原活化蛋白激酶
信号转导
MTT法
化学
脚踝
白细胞介素
分子生物学
内分泌学
内科学
细胞因子
医学
细胞
生物
转录因子
MAPK/ERK通路
生物化学
病理
基因
作者
Jie Shen,Rong Yao,Jing Mei,Zhiyu Zhou
出处
期刊:Medical Science Monitor
[International Scientific Information, Inc.]
日期:2018-09-21
卷期号:24: 6649-6655
被引量:8
摘要
BACKGROUND This study aimed to investigate the effects of SIN on ankle fracture and the underlying mechanisms in MG-63 cells. MATERIAL AND METHODS qRT-PCR and ELISA assay were used to detect the mRNA and protein levels of cytokines in peripheral blood of children with or without ankle fracture. The expression and activity of antioxidant and detoxifying enzymes were detected by ELISA assay. Pretreated MG-63 cells with/without SIN were stimulated with 1 μg/ml bradykinin (BK). A CCK-8 kit was used to detect the cell viability. The cytokines produced from MG-63 cells were detected by Western blotting and qRT-PCR. Moreover, Western blotting was used to detect the levels of p-p38 and p-NF-κB (p65), and the activation level of the Nrf2 signaling pathway was examined by qRT-PCR and Western blotting. RESULTS In this study, we found that compared with the healthy children, the mRNA and protein levels of interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α) were significantly upregulated in children with ankle fracture. In addition, the expression and activity of antioxidant and detoxifying enzymes were imbalanced in children with ankle fracture. SIN treatment did not have a cytotoxic effect on MG-63 cells. SIN dose-dependently suppressed BK-induced upregulation of IL-1β, IL-6, TNF-α, p-p38, and p-NF-κB (p65). Furthermore, SIN dramatically inhibited oxidative stress induced by BK via balancing the expression and activity of antioxidant and detoxifying enzymes and inhibited the activation of Nrf2 signaling. CONCLUSIONS SIN might be a potential agent for the treatment of ankle fracture through reducing inflammatory response and oxidative stress.
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