摘要
目的研究ATP敏感性钾通道(KATP)开放剂对人气道平滑肌细胞(HASMCs)肥大的影响及其可能的作用机制。方法用TGF-β1诱导HASMCs肥大,ATP敏感性钾通道开放剂尼可地尔(Nico)进行干预,将实验分成Control组、TGF-β1组、TGF-β1+Nico组、Nico组。显微镜下及免疫荧光法观察细胞形态变化及α-SMA表达情况;Western Blot法测定细胞α-SMA蛋白表达和CaMKⅡ、CREB磷酸化情况。结果免疫荧光实验表明TGF-β1能浓度依赖性地促进细胞肥大和α-SMA表达,Nico能下调α-SMA的表达,减轻细胞肥大;Western blot实验表明TGF-β1能升高α-SMA表达和CaMKⅡ、CREB磷酸化水平,Nico能抑制α-SMA的表达,降低CaMKⅡ、CREB磷酸化水平。结论 Nico能减轻TGF-β1诱导的HASMCs肥大,可能与抑制CaMKⅡ/CREB信号通路传导有关。
Objective To investigate the effects of the ATP sensitive potassium(KATP)channel openers on human airway smooth muscle cells(HASMCs)hypertrophy and the mechanism underlying.Methods The hypertrophy of HASMCs was induced by exposing to TGF-β1 in vitro.With the intervention of KATPchannel opener(Nicorandil),the experiment was divided into four groups:control group,TGF-β1 group,TGF-β1+ Nico group and Nico group.The cellular morphological changes and the expression ofα-SMA were observed by the microscope and immunofluorescence,the protein expression ofα-SMA and phosphorylation of CaMKⅡ,CREB were detected by Western blot.Results Nicorandil could suppress TGF-β1-induced HASMCs hypertrophy by reducing the expression ofα-SMA and phosphorylation of CaMKⅡ,CREB.Conclusion Nicorandil can inhibit TGF-β1-induced HASMCs hypertrophy by reducing the phosphorylation of CaMKⅡ/CREB signaling pathways.
作者
林昌建
LIN Changjian(Department of Pulmonary and Critical Care Medicine,Fujian Provincial Hospital,Fuzhou,Fujian 350001,China)
出处
《福建医药杂志》
CAS
2019年第1期109-112,共4页
Fujian Medical Journal
