Anti-Inflammatory Activities of Compounds Isolated from the Rhizome of Anemarrhena asphodeloides.
Anti-Inflammatory Activities of Compounds Isolated from the Rhizome of Anemarrhena asphodeloides.
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从Anemarrhena Asphodeloides的根茎分离的化合物的抗炎活性。
DOI：
10.3390/molecules23102631
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发表时间：
2018-10-13
期刊：
影响因子：
--
通讯作者：
Zhang C
中科院分区：
文献类型：
--
作者：
Wang Z;Cai J;Fu Q;Cheng L;Wu L;Zhang W;Zhang Y;Jin Y;Zhang C
从知母中分离得到15个未见报道的化合物，分别为：鸢尾酚（3）、玉簪皂苷C（7）、tuberoside G（8）、spicatoside B（9）、桔梗皂苷D（14）、桔梗皂苷A（15）、桔梗皂苷D2（16）、远志皂苷D2（17）、桔梗皂苷D3（18）、异牡荆素（20）、牡荆素（21）、3、4-二羟基烯丙基苯-3-O-α-L-吡喃鼠李糖基（1→6）-β-D-吡喃葡萄糖苷（22）、伊立普芬（24）、腺苷（25）、α-D-葡萄糖单烯丙基醚（26）以及11个已知化合物（1，2，4-6，10-13，19和23）。这些化合物的化学结构用HRMS和NMR表征。通过研究化合物抑制N9小胶质细胞中LPS诱导的NO产生的能力来评价化合物的抗炎活性。知母皂苷BIII（TBIII）和反式-扁柏树脂酚（t-HL）对NO的产生有明显的抑制作用，其IC_（50）值分别为11.91和39.08 μM，且呈剂量依赖性。免疫印迹显示TBIII和t-HL通过抑制LPS刺激的N9小胶质细胞中iNOS的表达来抑制NO的产生。进一步的研究结果显示，TBIII和t-HL预处理N9小胶质细胞可在mRNA和蛋白水平上减弱LPS诱导的肿瘤坏死因子（TNF）-α和白细胞介素-6（IL-6）的表达。此外，TBIII和t-HL分别抑制核因子-κB（NF-κB）和磷脂酰肌醇3-激酶（PI 3 K）/Akt信号通路的激活。我们的研究结果表明TBIII和t-HL对与神经炎症相关的神经退行性疾病的治疗意义。
Fifteen unreported compounds in Anemarrhena 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-α-l-rhamnopyranosyl(1→6)-β-d-glucopyranoside (22), iryptophan (24), adenosine (25), α-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 μM, 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)-α and interleukin-6 (IL-6) at mRNAs and protein levels. Moreover, the activation of nuclear factor-κB (NF-κB) 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.
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影响因子：
6.3
作者：
Kim DH;Chung JH;Yoon JS;Ha YM;Bae S;Lee EK;Jung KJ;Kim MS;Kim YJ;Kim MK;Chung HY
通讯作者：
Chung HY
影响因子：
5.4
作者：
Giles, James A.;Greenhalgh, Andrew D.;Davies, Claire L.;Denes, Adam;Shaw, Tovah;Coutts, Graham;Rothwell, Nancy J.;McColl, Barry W.;Allan, Stuart M.
通讯作者：
Allan, Stuart M.
影响因子：
4.8
作者：
Lee, H;Kim, YO;Suk, K
通讯作者：
Suk, K
影响因子：
2.7
作者：
Li, Su-Mei;Yang, Xian-Wen;Zhang, Wei-Dong
通讯作者：
Zhang, Wei-Dong
影响因子：
6.1
作者：
Jung, Ki Kyung;Lee, Hae Sung;Kang, Seog Youn
通讯作者：
Kang, Seog Youn