Inhibitory effects of honokiol on lipopolysaccharide-induced cellular responses and signaling events in human renal mesangial cells
Inhibitory effects of honokiol on lipopolysaccharide-induced cellular responses and signaling events in human renal mesangial cells
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和厚朴酚对人肾系膜细胞脂多糖诱导的细胞反应和信号转导事件的抑制作用。
DOI：
10.1016/j.ejphar.2010.11.022
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发表时间：
2011-03-01
影响因子：
5
通讯作者：
Li, Hong
中科院分区：
文献类型：
--
作者：
Wu, Fang;Zhang, Wei;Li, Hong
和厚朴酚已被证明具有许多药理功效，包括抗氧化、抗血管生成和抗肿瘤作用。在本研究中，我们研究了和厚朴酚的抗炎作用以及脂多糖（LPS）诱导的人肾系膜细胞（HRMC）状况中涉及的信号传导机制。当使用浓度为 40 μmol/l 时，和厚朴酚不会显着改变 HRMC 活力。在这项研究中，IPS 治疗导致 HRMC 中 IL-1β、IL-18、TNF-α、TGF-β1、CCL3、CCL3 和 CCL5 水平显着上调。 COX-2、iNOS及其产物PGE(2)和NO的表达也增加。这些分子的上调被和厚朴酚以剂量依赖性方式显着消除。此外，和厚朴酚在10μmol/l时几乎完全逆转IL-1β、CCL3和NO表达，在20μmol/l时几乎完全逆转IL-18、TNF-α、TGF-β1和COX-2表达。此外，在 LPS 处理的 HRMC 中，和厚朴酚显着抑制 Ser536 位点的磷酸化 NF-κ B p65、磷酸化 Akt 和磷酸化 p42/44。这些结果表明和厚朴酚可以抑制LPS诱导的HRMC中炎症细胞因子和介质的表达。和厚朴酚的抗炎机制部分归因于磷酸-NF-kappa B p65、磷酸-Akt 和磷酸-p42/44 通路的抑制。 (C) 2010 年由 Elsevier B.V. 出版
Honokiol has been shown to possess a lot of pharmacologic benefits, including antioxidative, antiangiogenic and antineoplastic effects. In the present study, we investigated the anti-inflammatory effects of honokiol and the signaling mechanisms involved in lipopolysaccharide (LPS)-induced conditions in human renal mesangial cells (HRMCs). Honokiol did not significantly change HRMC viability when used at a concentration of 40 mu mol/l. In this study, IPS treatment led to a marked upregulation of the levels of IL-1 beta, IL-18, TNF-alpha, TGF-beta 1, CCL3, CCL3, and CCL5 in HRMCs. The expression of COX-2, iNOS, and their products PGE(2) and NO also increased. The upregulation of these molecules was significantly abolished by honokiol in a dose-dependent manner. Moreover, honokiol almost completely reversed IL-1 beta, CCL3, and NO expression at 10 mu mol/l, and IL-18, TNF-alpha, TGF-beta 1, and COX-2 expression at 20 mu mol/l. In addition, phospho-NF-kappa B p65 at Ser536, phospho-Akt, and phospho-p42/44 were dramatically suppressed by honokiol in LPS-treated HRMCs. These results indicate that honokiol can inhibit the LPS-induced expression of inflammatory cytokines and mediators in HRMCs. The anti-inflammatory mechanisms of honokiol are partly due to the suppression of the phospho-NF-kappa B p65, phospho-Akt and phospho-p42/44 pathways. (C) 2010 Published by Elsevier B.V.