脂联素
内科学
受体
单核细胞
趋化因子
脂联素受体1
内分泌学
趋化性
化学
p38丝裂原活化蛋白激酶
信使核糖核酸
蛋白激酶A
四氯化碳
体外
激酶
生物
生物化学
医学
胰岛素抵抗
基因
胰岛素
作者
Tao Yao,Xiaoyan Wu,Wen-li Yu,Ping Gao
出处
期刊:Chin J Nephrol
日期:2015-02-15
卷期号:31 (2): 145-149
标识
DOI:10.3760/cma.j.issn.1001-7097.2015.02.012
摘要
Objective
To investigate the effect of globular adiponectin on the high expression of monocyte chemotactic protein-1 (MCP-1) induced by high glucose in rat renal tubular epithelial cells (NRK52E), and its relationship with adiponectin receptors and p38MAPK.
Methods
NRK52E cells were cultured in vitro and divided into six groups: normal glucose group (NG, 5.6 mmol/L glucose), high glucose group(HG, 25 mmol/L glucose), gAd group1 (HG+gAd 2 mg/L), gAd group2 (HG+gAd 5 mg/L), gAd group3 (HG+gAd 10 mg/L), p38MAPK antagonist group: (SB, HG+SB203580 10 μmol/L). The protein expression of phosphorylated p38MAPK (p-p38MAPK), total p38MAPK (t-p38MAPK), MCP-1 and AdipoR1/AdipoR2 were examined by western blotting. The mRNA expression of MCP-1 and AdipoR1/AdipoR2 were detected by RT-PCR and real-time PCR respectively.
Results
Compared with NG group, the mRNA and protein expression of MCP-1 increased significantly in HG group (all P 0.05). Compared to HG group, the mRNA and protein expression of adipoR1 increased in gAd groups (all P<0.01).
Conclusion
The gAd can dose-dependently attenuate the overexpression of MCP-1 induced by high glucose, and this protective effect may be mediated by adipoR1 and p38MAPK.
Key words:
Adiponectin; Receptors, adiponectin; Chemokine CCL2; p38 mitogen-activated protein kinases
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