The role of quinazoline in ameliorating intervertebral disc degeneration by inhibiting oxidative stress and anti-inflammation via NF-κB/MAPKs signaling pathway

炎症 氧化应激 椎间盘 喹唑啉 NF-κB 信号转导 化学 变性(医学) 细胞生物学 医学 生物 免疫学 生物化学 解剖 病理 立体化学
作者
Chen Zb,Yu Yb,Wa Qb,Zhou Jw,Helmut E. Meyer,Y. Cen
出处
期刊:DOAJ: Directory of Open Access Journals - DOAJ 被引量:20
链接
标识
摘要

Objective Previous studies have shown that Quinazoline (QNZ) plays extremely important roles in the cellular physiological activity, but it has been rarely examined on cell behavior following intervertebral disc degeneration (IVDD). The aim of this study was to investigate whether QNZ mediates oxidative stress and inflammation contributed to IL-1β-induced nucleus pulposus (NP) cells degeneration in vitro. Patients and methods NP were isolated cells from human disc samples collected from patients and the IL-1β-induced NP cells degenerated model was constructed. The cells were randomly divided into 3 groups, namely, Control group, IL-1β group (10 µM), QNZ + IL-1β group (containing 10 nM QNZ and 10 µM IL-1β). Then, the cell viability was determined by CCK-8 assay, and the levels of collagen I, collagen II, aggrecan, p16, p53, β-galactosidase (β-gal), antioxidant enzymes, 8-hydroxy-2-deoxyguanosine (8-OHdG), NF-κB/MAPKs signaling-related proteins and inflammatory factors were examined using Western blot and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) in NP cells. Finally, the expressions of IL-1β, IL-6, and TNF-α in the cell supernatants were also determined by enzyme-linked immunosorbent assay (ELISA). Results This study showed that IL-1β promoted the progress of IDD, with markedly increased expressions of collagen I, p16, p53, and β-gal, as well as decreased expressions of collagen II and aggrecan. However, QNZ treatment could reverse the effects of IL-1β. It was found that cell proliferation was increased, ROS level was decreased, antioxidant enzymes were upregulated, and inflammatory factors were reduced after QNZ stimulation. Moreover, NF-κB/MAPKs signaling proteins IKKβ, IκBα, p65, ERK, JNK, and p38 were significantly dephosphorylated by QNZ. Conclusions These results indicated that QNZ prevented NP degradation via restraining oxidative stress and inflammation through inhibition of the NF-κB/MAPKs signaling pathway. QNZ may become a novel insight into the therapy of IVDD in the future.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
77给77的求助进行了留言
刚刚
GMMY完成签到,获得积分20
刚刚
毛头侠发布了新的文献求助10
刚刚
范同学完成签到,获得积分10
1秒前
深情海安完成签到,获得积分20
1秒前
芯止谭轩完成签到,获得积分10
1秒前
顺顺完成签到,获得积分20
1秒前
Akim应助贺兰采纳,获得10
2秒前
horizon完成签到,获得积分20
2秒前
xiayiyi完成签到,获得积分10
2秒前
机会完成签到,获得积分10
2秒前
无望幽月完成签到,获得积分10
2秒前
Ghost完成签到,获得积分10
3秒前
randylch完成签到,获得积分0
3秒前
3秒前
小香草发布了新的文献求助20
3秒前
愉快迎南完成签到,获得积分10
3秒前
4秒前
原原完成签到,获得积分10
4秒前
satori完成签到,获得积分10
4秒前
4秒前
zhaojian完成签到,获得积分20
4秒前
4秒前
5秒前
芋圆完成签到,获得积分10
5秒前
嘚嘚嘚发布了新的文献求助10
5秒前
夜雨完成签到,获得积分10
5秒前
江海下百川完成签到,获得积分10
5秒前
量子星尘发布了新的文献求助10
6秒前
WANG.完成签到,获得积分10
7秒前
kaiX完成签到,获得积分10
7秒前
7秒前
在水一方应助菲菲呀采纳,获得10
7秒前
7秒前
认真初南发布了新的文献求助10
7秒前
Tina完成签到,获得积分10
7秒前
8秒前
一周发布了新的文献求助10
8秒前
ZJ完成签到,获得积分10
9秒前
幸福大白发布了新的文献求助10
9秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
网络安全 SEMI 标准 ( SEMI E187, SEMI E188 and SEMI E191.) 1000
计划经济时代的工厂管理与工人状况(1949-1966)——以郑州市国营工厂为例 500
INQUIRY-BASED PEDAGOGY TO SUPPORT STEM LEARNING AND 21ST CENTURY SKILLS: PREPARING NEW TEACHERS TO IMPLEMENT PROJECT AND PROBLEM-BASED LEARNING 500
Why America Can't Retrench (And How it Might) 400
Two New β-Class Milbemycins from Streptomyces bingchenggensis: Fermentation, Isolation, Structure Elucidation and Biological Properties 300
Modern Britain, 1750 to the Present (第2版) 300
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 纳米技术 计算机科学 内科学 化学工程 复合材料 物理化学 基因 催化作用 遗传学 冶金 电极 光电子学
热门帖子
关注 科研通微信公众号,转发送积分 4614444
求助须知:如何正确求助?哪些是违规求助? 4018649
关于积分的说明 12439260
捐赠科研通 3701425
什么是DOI,文献DOI怎么找? 2041187
邀请新用户注册赠送积分活动 1073927
科研通“疑难数据库(出版商)”最低求助积分说明 957600