Department of Prescriptionology, College of Oriental Medicine, Institute of Oriental Medicine, Kyung Hee University, Seoul 130-701, Republic of Korea.
J Ethnopharmacol. 2013 Sep 16;149(2):506-12. doi: 10.1016/j.jep.2013.07.008. Epub 2013 Jul 18.
Rhizoma coptidis (RC) has been used as a remedy for inflammation-related diseases in traditional medicine. Although it is known to have anti-inflammatory activities, its mechanism of action on lipopolysaccharide (LPS)-induced inflammation has not yet been identified in detail.
This study was designed to assess the beneficial effects of pretreatment with RC in ameliorating LPS-induced liver inflammation.
Mice were orally administered RC (500, 1000 mg/kg) for three days in a row. 1h after the last RC administration, the mice were intraperitoneally injected with LPS (35 mg/kg). After treatment, histological alterations and inflammatory factor levels in the liver and proinflammatory cytokines in the serum associated with inflammation were examined.
We found that pretreatment with RC (500 and 1000 mg/kg) exerted a significant protective effect by attenuating liver histopathological changes in endotoxemic mice. The results also demonstrated that RC suppressed secretion of LPS-stimulated pro-inflammatory cytokines, such as interleukin-6 (IL-6). Furthermore, RC inhibited LPS-mediated nuclear factor (NF)-κB activation via the prevention of IκB-α phosphorylation, as well as the phosphorylation of ERK1/2, JNK, and p38 MAPKs. These results were associated with decreases in the expression of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (I-NOS).
The results presented here clearly demonstrate that RC could significantly protect mice against LPS-induced acute liver injury.
黄连（RC）在传统医学中已被用作治疗与炎症相关的疾病的药物。虽然已知其具有抗炎活性，但它对脂多糖（LPS）诱导的炎症的作用机制尚未得到详细阐明。
本研究旨在评估 RC 预处理对改善 LPS 诱导的肝炎症的有益作用。
连续三天，将小鼠经口给予 RC（500、1000mg/kg）。末次 RC 给药 1 小时后，小鼠腹腔内注射 LPS（35mg/kg）。治疗后，检查肝组织学改变和 LPS 诱导的肝炎症相关的炎症因子水平以及血清中促炎细胞因子。
我们发现，RC（500 和 1000mg/kg）预处理通过减轻内毒素血症小鼠的肝组织病理学变化发挥了显著的保护作用。结果还表明，RC 抑制了 LPS 刺激的促炎细胞因子（如白细胞介素-6（IL-6））的分泌。此外，RC 通过防止 IκB-α磷酸化以及 ERK1/2、JNK 和 p38 MAPKs 的磷酸化，抑制了 LPS 介导的核因子（NF）-κB 激活。这些结果与环加氧酶-2（COX-2）和诱导型一氧化氮合酶（I-NOS）的表达减少有关。
本研究结果清楚地表明，RC 可显著保护小鼠免受 LPS 诱导的急性肝损伤。
