Icariin is the main active compound extracted from epimedium Flavonoids (EFs) and involved in regulation of cell behaviors (proliferation, apoptosis, and autophagy etc.) for many cell types, but the effect of Icariin on airway smooth muscle cells (ASMCs) is still unknown. The aim of the present study is to examine the role of Icariin on rat ASMCs proliferation, apoptosis and autophagy. CKK8 assay showed that Icariin inhibited rat ASMCs growth in dose-time-dependent manner, and the flow cytometry assay showed that the Icariin interfered with ASMCs cell cycle, when treated with Icariin, S phase shortened while G2 phase extended, cyclin E1 and cyclinA1 gene and protein expression decreased. Next apoptosis was detected, Flow cytometry and TdTmediated dUTP Nick-End Labeling (TUNEL) assay showed that Icariin promoted ASMCs apoptosis, and enhanced apoptosis protein cleaved-caspase-3 expression. Finally, it was found Icariin induced rat ASMCs autophagy, with enhancement expression of autophagy marker LC3 II. In conclusion, Icariin inhibited ASMCs proliferation while promoted apoptosis and autophagy, revealing its potential role in treatment of airway remodeling in asthma.

中文翻译：

---

生物活性分子鹰嘴豆素抑制增殖，同时增强大鼠气道平滑肌细胞的凋亡和自噬。

鹰嘴豆素是从淫羊Fla类黄酮（EFs）中提取的主要活性化合物，并参与许多细胞类型的细胞行为（增殖，凋亡和自噬等）的调节，但鹰嘴豆素仍对气道平滑肌细胞（ASMCs）产生影响。未知。本研究的目的是研究伊卡瑞林对大鼠ASMC增殖，凋亡和自噬的作用。CKK8检测结果表明，叶黄素以剂量-时间依赖性的方式抑制大鼠ASMCs的生长，流式细胞仪检测表明，叶黄素对ISMC的细胞周期有干扰作用，经叶黄素处理后S期缩短，G2期延长，cyclin E1和cyclinA1基因和蛋白质表达下降。检测到下一个细胞凋亡，流式细胞仪和TdT介导的dUTP缺口末端标记（TUNEL）分析表明，叶黄素可促进ASMC凋亡，并增强凋亡蛋白裂解的caspase-3表达。最后，发现了鹰嘴豆素诱导的大鼠ASMC自噬，并增强了自噬标记物LC3 II的表达。总之，鹰嘴豆素抑制ASMCs增殖，同时促进细胞凋亡和自噬，显示其在治疗哮喘气道重塑中的潜在作用。