摘要：
Phytochemical investigation of the fresh tubers of Ophiopogon japonicus led to the isolation of two new furostanol saponins (1 and 2) together with two known steroidal saponins (3 and 4). Comprehensive spectroscopic analysis allowed the chemical structures of two new compounds to be elucidated as (25R)-26-O-[beta-d-glucopyranosyl-(1 --> 2)-beta-d-glucopyranosyl]-5-ene-furost-1beta,3beta,22alpha,26-tetraol-3-O-alpha-l -rhamnopyranosyl-(1 --> 2)-[beta-d-xylopyranosyl-(1 --> 4)]-beta-d-glucopyranoside (1, ophiopogonin P) and (25R)-26-O-[beta-d-glucopyranosyl-(1 --> 6)-beta-d-glucopyranosyl]-5-ene-furost-1beta,3beta,22alpha,26-tetraol-3-O-alpha-l -rhamnopyranosyl-(1 --> 2)-[beta-d-xylopyranosyl-(1 --> 4)]-beta-d-glucopyranoside (2, ophiopogonin Q). Furostanol saponins with the disaccharide chain linked at C-26 hydroxy group of the aglycone have been rarely reported from natural sources.
作者机构：
[Li, Lifang] Univ South China, Dept Microbiol & Immunol, Hengyang 421001, Peoples R China.;[Xie, Feng; Guo, Yu; Li, Lanfang; Lv, Deguan; Lu, Qixuan; Tang, Guotao; Chen, Linxi] Univ South China, Inst Pharm & Pharmacol, Learning Key Lab Pharmacoprote, Hengyang 421001, Peoples R China.;[Zhang, Zidong] Univ Mississippi, Med Ctr, Dept Microbiol, Jackson, MS 39216 USA.;[Li, Jian] Beijing Hosp, Key Lab Geriatr, Beijing 100730, Peoples R China.;[Li, Jian] Minist Hlth, Beijing Inst Geriatr, Beijing 100730, Peoples R China.
通讯机构：
[Chen, Linxi] U;Univ South China, Inst Pharm & Pharmacol, Learning Key Lab Pharmacoprote, Hengyang 421001, Peoples R China.
关键词：
G protein-coupled receptor;cell proliferation;vascular smooth muscle cell;Jagged-1/Notch3
摘要：
The apelin/apelin receptor (APJ, apelin–angiotensin receptor-like 1) system is a newly deorphanized G protein-coupled receptor system. Both apelin and APJ that are important regulatory factors are expressed in the cardiovascular system. Our previous studies demonstrated that apelin-13 significantly stimulated vascular smooth muscle cell (VSMC) proliferation. In this paper, our data suggested that the Jagged-1/Notch3 signaling transduction pathway is involved in apelin-13-induced VSMC proliferation by promoting the expression of Cyclin D1. Results indicated that apelin-13 stimulates the proliferation of VSMC and the expression of Jagged-1 and Notch3 in concentration- and time-dependent manners. The increased expression of Jagged-1 and Notch3 induced by apelin-13 could be abolished by extracellular signal-regulated protein kinase (ERK) blockade. PD98059 (ERK inhibitor) can inhibit the activation of Jagged-1/Notch3 induced by apelin-13. Down-regulation of Notch3 using small interfering RNA inhibits the expression of Cyclin D1 and prevents apelin-13-induced VSMC proliferation. In conclusion, Jagged-1/Notch3 signaling transduction pathway is involved in VSMC proliferation induced by apelin-13.
作者机构：
[李兰芳; 李峰; 杨莉; 毛小环; 柳威; 谢凤; 秦旭平; 郭玉; 陈临溪] Institute of Pharmacy and Pharmacology,University of South China;[李兰芳; 李峰; 杨莉; 毛小环; 柳威; 谢凤; 秦旭平; 郭玉; 陈临溪] Department of Physiology,Hunan College of Traditional Chinese Medicine;[李兰芳; 李峰; 杨莉; 毛小环; 柳威; 谢凤; 秦旭平; 郭玉; 陈临溪] Institute of Pharmacy and Pharmacology,University of South China,
会议名称：
中国活性氧生物学效应学术会议
会议时间：
2011-09-01
会议地点：
中国陕西西安
会议论文集名称：
中国活性氧生物学效应学术会议论文集（第一册）
摘要：
<正>Apelin is the endogenous ligand of the G protein coupled receptor,APJ.Vascular smooth muscle cells express both apelin and APJ,which are important regulatory factors in the cardiovascular systems. Previourly we reported that apelin-13 significantly stimulated vascular smooth muscle cell proliferation. However,little is known about the precise cellular mechanisms responsible for vascular smooth muscle cell proliferation induced by apelin-13.Here,we present novel data that indicate the key role of NADPH oxidase-derived reactive oxygen species in vascular smooth muscle cell proliferation treated by apelin-13. Apelin-13 stimulated reactive oxygen species production in a concentration and time-dependent manner. And DPI,a NADPH oxidase inhibitor,impaired apelin-13-induced reactive oxygen species generation and vascular smooth muscle cells proliferation.Apelin-13-treatment increased the expression of NADPH oxidase 4 in a dose-dependent manner.Down-regulation of NADPH oxidase 4 using siRNA prevented apelin-13-induced reactive oxygen species generation and vascular smooth muscle cells proliferation.An increase in reactive molecules can trigger the activation of ERKl/2 stress-sensitive signaling pathways but not P38 and JNK.In conclusion,Apelin-13 induced the vascular smooth muscle cells proliferation by NOX4-derived ROS via ERK1/2 signal pathway.
