Astragaloside IV inhibits NF- κ B activation and inflammatory gene expression in LPS-treated mice.
Astragaloside IV inhibits NF- κ B activation and inflammatory gene expression in LPS-treated mice.
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DOI：
10.1155/2015/274314
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发表时间：
2015
影响因子：
4.6
通讯作者：
Frei B
中科院分区：
文献类型：
--
作者：
Zhang WJ;Frei B
本研究探讨了黄芪皂苷IV（AS-IV）对LPS诱导的小鼠急性炎症反应的影响及其可能的机制。将小鼠分为四组：溶媒给药对照动物; AS-IV给药动物（10 mg/kg b.w. AS-IV每日腹膜内注射6天）; LPS处理的动物;和AS-IV加LPS处理的动物。我们发现，AS-IV治疗显着抑制LPS诱导的血清MCP-1和TNF水平的增加，分别为82%和49%。AS-IV还抑制LPS诱导的不同器官中炎症基因表达的上调。AS-IV预处理小鼠后，细胞粘附分子MCP-1、TNF α、IL-6和TLR4的肺mRNA水平显著降低，肺中性粒细胞浸润和活化受到强烈抑制，表现为髓过氧化物酶含量降低。在心脏、主动脉、肾脏和肝脏中观察到类似的结果。此外，AS-Ⅳ还能显著抑制LPS诱导的肺和心脏NF-κ B和AP-1的DNA结合活性。总之，我们的数据提供了新的体内证据，即AS-IV通过调节NF-κ B和AP-1信号通路有效地抑制LPS诱导的急性炎症反应。我们的研究结果表明，AS-IV可能是有用的预防或治疗炎症性疾病。
In this study we investigated the role of astragaloside IV (AS-IV), one of the major active constituents purified from the Chinese medicinal herb Astragalus membranaceus, in LPS-induced acute inflammatory responses in mice in vivo and examined possible underlying mechanisms. Mice were assigned to four groups: vehicle-treated control animals; AS-IV-treated animals (10 mg/kg b.w. AS-IV daily i.p. injection for 6 days); LPS-treated animals; and AS-IV plus LPS-treated animals. We found that AS-IV treatment significantly inhibited LPS-induced increases in serum levels of MCP-1 and TNF by 82% and 49%, respectively. AS-IV also inhibited LPS-induced upregulation of inflammatory gene expression in different organs. Lung mRNA levels of cellular adhesion molecules, MCP-1, TNFα, IL-6, and TLR4 were significantly attenuated, and lung neutrophil infiltration and activation were strongly inhibited, as reflected by decreased myeloperoxidase content, when the mice were pretreated with AS-IV. Similar results were observed in heart, aorta, kidney, and liver. Furthermore, AS-IV significantly suppressed LPS-induced NF-κB and AP-1 DNA-binding activities in lung and heart. In conclusion, our data provide new in vivo evidence that AS-IV effectively inhibits LPS-induced acute inflammatory responses by modulating NF-κB and AP-1 signaling pathways. Our results suggest that AS-IV may be useful for the prevention or treatment of inflammatory diseases.
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DOI：
10.1161/01.atv.0000143096.15099.ce
发表时间：
2004-10-01
影响因子：
8.7
作者：
Schabbauer, G;Tencati, M;Mackman, N
通讯作者：
Mackman, N
影响因子：
3.7
作者：
Fu S;Zhang J;Menniti-Ippolito F;Gao X;Galeotti F;Massari M;Hu L;Zhang B;Ferrelli R;Fauci A;Firenzuoli F;Shang H;Guerra R;Raschetti R
通讯作者：
Raschetti R
DOI：
10.1007/bf03190631
发表时间：
2005-10-01
影响因子：
1.9
作者：
Du, Y;Zhang, Q;Tu, CY
通讯作者：
Tu, CY
影响因子：
3.7
作者：
Denzler KL;Waters R;Jacobs BL;Rochon Y;Langland JO
通讯作者：
Langland JO
影响因子：
5.4
作者：
Ryu, Minsook;Kim, Eun Hye;Lee, Jong-Soo
通讯作者：
Lee, Jong-Soo