首页> 美国卫生研究院文献>Evidence-based Complementary and Alternative Medicine : eCAM >Protective Effect of Jianpiyifei II Granule against Chronic Obstructive Pulmonary Disease via NF-κB Signaling Pathway
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Protective Effect of Jianpiyifei II Granule against Chronic Obstructive Pulmonary Disease via NF-κB Signaling Pathway

机译:健脾益肺Ⅱ号颗粒通过NF-κB信号通路对慢性阻塞性肺疾病的保护作用

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摘要

Jianpiyifei II granule (JPYF II) is an oriental herbal formula used clinically in China to treat chronic obstructive pulmonary disease (COPD). The aim of the present study was to investigate the anti-inflammatory and antioxidative activities of JPYF II in a mouse model of COPD induced by lipopolysaccharide (LPS) and cigarette smoke (CS) and in RAW264.7 cells stimulated with cigarette smoke extract (CSE). Mice were given LPS via intratracheal instillation on days 1 and 15 and exposed to CS generated from 4 cigarettes/day for 28 days. The mice were treated with 0.75, 1.5, or 3 g/kg/d JPYF II by intragastric administration in low, middle, and high dose groups, respectively, for two weeks. RAW264.7 cells were stimulated by CSE and treated with JPYF II at doses of 12.5, 25, or 50 μg/mL. In the mouse model of LPS and CS-induced COPD, JPYF II decreased inflammatory cell counts in broncho alveolar lavage fluid (BALF), in addition to mRNA expression of proinflammatory cytokines and metalloproteinases (MMPs) in lung tissues. In addition, JPYF II elevated catalase (CAT) and glutathione peroxidase (GSH-Px) activities and reduced the levels of malondialdehyde (MDA) and IκBα and p65 phosphorylation and inflammatory cell infiltration in the lung tissues. In RAW264.7 cells stimulated with CSE, JPYF II inhibited the mRNA levels of inflammatory mediators and the phosphorylation of IκBα and p65. Our results suggest that JPYF II enhanced anti-inflammatory and antioxidative activities in a mouse model of COPD induced by LPS and CS and in RAW264.7 cells stimulated with CSE via inhibition of the NF-κB pathway.
机译:健脾益肺II颗粒(JPYF II)是一种东方草药配方,在中国临床用于治疗慢性阻塞性肺疾病(COPD)。本研究的目的是研究JPYF II在脂多糖(LPS)和香烟烟雾(CS)诱导的COPD小鼠模型中以及香烟烟雾提取物(CSE)刺激的RAW264.7细胞中的抗炎和抗氧化活性)。在第1天和第15天通过气管内滴注对小鼠给予LPS,并使其暴露于每天4支香烟产生的CS中28天。通过在低,中和高剂量组中通过胃内给药分别用0.75、1.5或3μg/ kg / d JPYF II治疗小鼠两周。用CSE刺激RAW264.7细胞,并以12.5、25或50μg/ mL的剂量用JPYF II处理。在LPS和CS诱导的COPD的小鼠模型中,除了肺组织中促炎细胞因子和金属蛋白酶(MMP)的mRNA表达外,JPY II减少了支气管肺泡灌洗液(BALF)中的炎症细胞计数。此外,JPY II提高了过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)的活性,并降低了肺组织中丙二醛(MDA)和IκBα的水平以及p65磷酸化和炎性细胞浸润。在CSE刺激的RAW264.7细胞中,JPY II抑制炎症介质的mRNA水平以及IκBα和p65的磷酸化。我们的结果表明,在抑制LPS和CS诱导的COPD小鼠模型中以及在CSE刺激的RAW264.7细胞中,JPF II通过抑制NF-κB途径增强了抗炎和抗氧化活性。

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