阿格里坎
椎间盘
变性(医学)
p38丝裂原活化蛋白激酶
MAPK/ERK通路
污渍
化学
细胞生物学
细胞外基质
体内
白细胞介素
分子生物学
信号转导
细胞因子
病理
医学
内科学
生物
解剖
生物化学
骨关节炎
基因
替代医学
生物技术
关节软骨
作者
Jun Ge,Qi Yan,Yingjie Wang,Xiaoqiang Cheng,Dawei Song,Cenhao Wu,Hao Yu,Huilin Yang,Jun Zou
标识
DOI:10.1016/j.freeradbiomed.2019.12.040
摘要
The degeneration of intervertebral discs (IVD) is a risk factor for chronic low back pain. Anti-inflammation therapy could alleviate IVD degeneration. IL-10 is an important anti-inflammatory cytokine. However, the effect of IL-10 on IVD has not been fully revealed. The current study is to reveal the effect of IL-10 on IVD and its underlying mechanism.IL-1β was used to induce the degeneration of nucleus pulposus cells (NPCs). mRNA expression level was determined by qPCR. Protein expression level was determined by western blotting. Methylene blue was used to determined the expression of aggrecan. Immunocytochemical staining was used to determined the expression of collagen II. A rat caudal IVD degeneration model was established and used to evaluate the effect of IL-10 on IVD in vivo.IL10 could alleviated NPC degeneration in both morphology and extracellular matrix. IL-10 could increase the mRNA expression of Collagen II, Sox-9, but decrease the mRNA expression of IL-1β, TNFα and Collagen X. IL-10 could also increase the protein level of Collagen II and aggrecan, but decrease that of Collagen X. Western blotting futher revealed the mechanism of the positive effect of IL-10 on IVD. IL-10 reduces phosphorylation level of p38 MAPK effectively. Rat caudal IVD degeneration model futher confirmed the positive effect of IL-10 on IVD degeneration and its mechanism in vivo.The current study demonstrates that exogenous IL-10 treatment can induce an anti-inflammatory response and inhibit p38 MAPK activation to delay IVD degeneration.
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