CTGF公司
纤维连接蛋白
MAPK/ERK通路
纤维化
转化生长因子
细胞外基质
化学
污渍
下调和上调
p38丝裂原活化蛋白激酶
激酶
生长因子
受体
分子生物学
内分泌学
内科学
医学
生物
生物化学
基因
作者
Wang Qj,Zhang Al,Kang Zq,Zhang Zt,Wang Ys
出处
期刊:PubMed
日期:2019-09-01
卷期号:23 (17): 7184-7190
被引量:8
标识
DOI:10.26355/eurrev_201909_18819
摘要
To evaluate the effect of interleukin-19 (IL-19) treatment on epidural fibrosis and its mechanism of action with transforming growth factor β (TGF-β).Initially, IL-19 (10, 20, 50 and 100 ng/L) was used to pretreat rat fibroblasts. TGF-β (10 μg/L) was then applied to activate fibroblasts. The protein expression levels of TGF-β receptor, extracellular-signal-regulated kinase (Erk) and p-38 were measured by Western blotting. In addition, we performed laminectomy at T10 vertebral plate in rats, followed by injection of IL-19 in caudal vein one week after injury. Furthermore, IL-19, TGF-β and fibrosis indexes were measured by quantitative Real-time polymerase chain reaction (qRT-PCR) and Western blotting at 7 and 28 days after injury, respectively.Concentration-dependent IL-19 significantly down-regulated TGF-β receptor expression and inhibited phosphorylated Erk (p-Erk) and phosphorylated p38 (p-p38). In vivo, IL-19 reduced the expressions of TGF-β and connective tissue growth factor (CTGF) at 7 days. Furthermore, IL-19 significantly suppressed extracellular matrix productions formation, including α smooth muscle actin (α-SMA) and collagen-1 (COL-1), and fibronectin at 28 days.IL-19 inhibited TGF-β expression via Erk and p38 pathway. Moreover, it decreased CTGF expression to suppress α-SMA, COL-1 and fibronectin in scar tissues, thereby preventing spinal cord from compression of scar tissues.
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