摘要
目的探讨ERK1/2通路在IL-33激活心脏成纤维细胞中的表达及其作用。方法培养心脏成纤维细胞,10 ng/m L IL-33刺激细胞,不同时间点MTT法检测IL-33对心脏成纤维细胞增殖的影响;RT-PCR检测细胞标志性基因α-SMA及通路关键分子TRAF-6的m RNA表达水平;Western blot检测α-SMA、TRAF-6及p-ERK1/2和ERK1/2的蛋白表达。结果 IL-33能促进心脏成纤维细胞的增殖(P<0.05);IL-33刺激细胞24h,TRAF-6表达显著上调(P<0.05),p-ERK1/2蛋白水平表达明显高于对照组(P<0.05);IL-33干预24h后α-SMA表达明显上调(P<0.05),ERK1/2特异性阻断剂PD98059可有效抑制该效应。结论ERK1/2通路参与了IL-33诱导的心脏成纤维细胞增殖和纤维化过程。
Objective To explore the role of ERK1/2 in the process of IL-33-induced activation of CFBs. Methods Culturing and stimulating CFBs cells with 10 ng/m L IL-33 at different time points, the proliferation of CFBs cells was tested by MTT; RT-PCR detected changes of genes α-SMA m RNA and critical signal transducer TRAF-6 m RNA;Western blotting was used to test the protein expression of α-SMA、TRAF-6、p-ERK1/2 and ERK1/2. Results The data showed that IL-33 had an effect on proliferation of CFBs cells（P0.05）; After CFBs were treated for 24 h, the expression of TRAF-6 was up-regulated（P0.05） and the protein level of p-ERK1/2 was significantly increased（P0.05）;Treatment cells with IL- 33 for 24 h the expression of α- SMA was up- regulated（ P 0. 05）, but ERK1 / 2 inhibitor PD98059 significantly abrogated the effect of IL-33. Conclusion The activation of ERK1/2 signaling pathway might be involved in the process of IL-33-induced proliferation of CFBs and fibrosis.
出处
《中国现代医生》
2014年第34期4-7,共4页
China Modern Doctor
基金
浙江省宁波市自然科学基金资助项目(2014A610276
2014A610271)
