文献类型：期刊文献

英文题名：Anti-Inflammatory Activities of Compounds Isolated from the Rhizome of Anemarrhena asphodeloides

作者：Wang, Zeyuan[1];Cai, Jianfeng[2];Fu, Qing[2];Cheng, Lingping[2];Wu, Lehao[3];Zhang, Weiyue[3];Zhang, Yan[3];Jin, Yu[2];Zhang, Chunzhi[1]

机构：[1]Dalian Polytech Univ, Sch Biol Engn, Dalian 116034, Peoples R China;[2]East China Univ Sci & Technol, Sch Pharm, Engn Res Ctr Pharmaceut Proc Chem, Minist Educ, Shanghai 200237, Peoples R China;[3]Shanghai Jiao Tong Univ, Sch Pharm, Shanghai 200240, Peoples R China

年份：2018

卷号：23

期号：10

外文期刊名：MOLECULES

收录：;WOS:【SCI-EXPANDED(收录号:WOS:000451201400227)】；

基金：This research was funded by Fundamental Research Funds for the Central Universities (222201717016).

语种：英文

外文关键词：Anemarrhena asphodeloides; purification; anti-inflammation; N9

摘要：Fifteen unreported compounds in WAnemarrhena asphodeloides, iriflophene (3), hostaplantagineoside C (7), tuberoside G (8), spicatoside B (9), platycodin D (14), platycoside A (15), platycodin D2 (16), polygalacin D2 (17), platycodin D3 (18), isovitexin (20), vitexin (21), 3,4-dihydroxyallylbenzene-3-O-alpha-L-rhamnopyranosyl(1 -> 6)-beta-D-glucopyranoside (22), iryptophan (24), adenosine (25), alpha-D-Glucose monoallyl ether (26), together with eleven known compounds (1, 2, 4-6, 10-13, 19 and 23), were isolated from the rhizomes of Anemarrhena asphodeloides. The chemical structures of these compounds were characterized using HRMS and NMR. The anti-inflammatory activities of the compounds were evaluated by investigating their ability to inhibit LPS-induced NO production in N9 microglial cells. Timosaponin BIII (TBIII) and trans-hinokiresinol (t-HL) exhibited significant inhibitory effects on the NO production in a dose-dependent manner with IC50 values of 11.91 and 39.08 mu M, respectively. Immunoblotting demonstrated that TBIII and t-HL suppressed NO production by inhibiting the expressions of iNOS in LPS-stimulated N9 microglial cells. Further results revealed that pretreatment of N9 microglial cells with TBIII and t-HL attenuated the LPS-induced expression tumor necrosis factor (TNF)-alpha and interleukin-6 (IL-6) at mRNAs and protein levels. Moreover, the activation of nuclear factor-kappa B (NF-kappa B) and phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways were inhibited by TBIII and t-HL, respectively. Our findings indicate that the therapeutic implication of TBIII and t-HL for neurogenerative disease associated with neuroinflammation.