Department of Pharmacology, School of Medicine, Graduate Institute of Basic Medical Science and Tsuzuki Institute for Traditional Medicine, China Medical University, 91 Hsueh Shih Road, Taichung, Taiwan.
J Ethnopharmacol. 2011 Apr 26;135(1):116-25. doi: 10.1016/j.jep.2011.02.031. Epub 2011 Mar 4.
The entire plant of Ajuga bracteosa Wall has been used to treat various inflammatory disorders, including hepatitis, in Taiwan.
This study evaluated the hepatoprotective ability of Ajuga bracteosa extract (ABE).
We investigated the inhibitory action of a chloroform fraction of ABE (ABCE) on lipopolysaccharide (LPS)-stimulated RAW264.7 cells and Kupffer cells. Hepatic fibrosis was induced in mice through the administration of CCl(4) twice a week for 8 weeks. Mice in three CCl(4) groups were treated daily with water and ABE throughout the duration of the experiment.
In LPS-stimulated RAW264.7 cells and Kupffer cells, ABCE inhibited the production of NO and/or TNF-α and also blocked the LPS-induced expression of NO synthase. ABCE inhibited the activation of NF-κB induced by LPS, associated with the abrogation of IκBα degradation, with a subsequent decrease in nuclear p65 and p50 protein levels. The phosphorylation of MAPKs in LPS-stimulated RAW264.7 cells was also suppressed using ABCE. In the in vivo study, ABE protected the liver from injury by reducing the activity of plasma aminotransferase, and by improving the histological architecture of the liver. RT-PCR analysis showed that ABE inhibited the hepatic mRNA expression of LPS binding protein, CD14, TNF-α, collagen(α1)(I), and α-smooth actin.
These results indicate that ABE alleviated CCl(4)-induced liver fibrosis, and that this protection is probably due to the suppression of macrophage activation.
在台湾,白花丹全草被用于治疗各种炎症性疾病,包括肝炎。
本研究评估了白花丹提取物(ABE)的保肝作用。
我们研究了 ABE 的氯仿部分(ABCE)对脂多糖(LPS)刺激的 RAW264.7 细胞和枯否细胞的抑制作用。通过每周两次给予 CCl4 共 8 周诱导小鼠肝纤维化。在 CCl4 三组实验中,各组小鼠在整个实验过程中每日用水和 ABE 处理。
在 LPS 刺激的 RAW264.7 细胞和枯否细胞中,ABCE 抑制了 NO 和/或 TNF-α的产生,并阻断了 LPS 诱导的一氧化氮合酶表达。ABCE 抑制了 LPS 诱导的 NF-κB 激活,与 IκBα降解的阻断有关,随后降低了核 p65 和 p50 蛋白水平。ABCE 还抑制了 LPS 刺激的 RAW264.7 细胞中 MAPKs 的磷酸化。在体内研究中,ABE 通过降低血浆转氨酶活性和改善肝组织学结构来保护肝脏免受损伤。RT-PCR 分析表明,ABE 抑制了 LPS 结合蛋白、CD14、TNF-α、胶原(α1)(I)和α-平滑肌肌动蛋白的肝 mRNA 表达。
这些结果表明,ABE 减轻了 CCl4 诱导的肝纤维化,这种保护作用可能是由于抑制了巨噬细胞的激活。