摘要
目的探讨桃叶珊瑚苷对脂多糖所致血管内皮细胞损伤的保护作用。方法采用细菌脂多糖(LPS)诱导人脐静脉血管内皮细胞(HUVECs)损伤模型,经桃叶珊瑚苷(25、50、100μmol·L^-1)处理后,以乳酸脱氢酶(LDH)漏出法检测细胞损伤情况,RT-q PCR检测促炎症因子mRNA的表达水平,Western Blotting法检测炎症相关蛋白及激酶的表达水平。结果桃叶珊瑚苷(50、100μmol·L^-1)能明显抑制LPS所致的HUVECs细胞损伤,呈现一定的剂量依赖性。同时,桃叶珊瑚苷(50、100μmol·L^-1)也能明显抑制白细胞介素1β、白细胞介素6mRNA的表达及LPS诱导的一氧化氮合酶、环氧化酶2蛋白的表达。此外,在50、100μmol·L^-1剂量下,桃叶珊瑚苷还能减弱LPS诱导的ERK1/2、p38 MAPK及JNK的磷酸化。结论桃叶珊瑚苷对LPS所致HUVECs损伤具有一定保护作用,其机制可能与抑制MAPKs炎症信号通路有关。
OBJECTIVE To study the protective effect of aucubin against lipopolysaccharide( LPS)-induced human umbilical vein endothelial cells( HUVECs) injury. METHODS HUVECs were pretreated with aucubin,and then exposed to LPS for 24 h. Lactate dehydrogenase( LDH) leak assay was used to test the cell viability of HUVECs. The mRNA levels of interleukin 1β( IL-1β) and interleukin 6( IL-6) were evaluated by RT-q PCR. The phosphorylation levels of inflammation-associated kinases were measured by western blot. RESULTS Aucubin significantly inhibited LPS-induced HUVECs injury in a dose-dependent manner. Furthermore,aucubin also obviously attenuated the mRNA levels of IL-1β and IL-6,as well as the protein expressions of i NOS and COX2,respectively. Finally,the elevated phosphorylation levels of ERK1/2,p38 MAPK,and JNK were blocked by aucubin treatment. CONCLUSION Aucubin possesses a protective effect against LPS-induced HUVEC injury through suppression of MAPKs signaling.
作者
沈晓飞
王祎
SHEN Xiaofei;WANG Yi(Institute of Maternal and Child Medicine,West China Second University Hospital,Sichuan University,Chengdu,Sichuan, 610041 P.R. China;West China College of Basic and Forensic Medicine,Sichuan University,610041,Chengdu,Sichuan, 610041 P.R. China)
出处
《华西药学杂志》
CAS
CSCD
2019年第5期458-462,共5页
West China Journal of Pharmaceutical Sciences