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Immunomodulatory Effect of Chinese Herbal Medicine Formula Sheng-Fei-Yu-Chuan-Tang in Lipopolysaccharide-Induced Acute Lung Injury Mice

机译:中国草药甲盛富川曲中的免疫调节作用脂多糖诱导的急性肺损伤小鼠

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摘要

Traditional Chinese medicine formula Sheng-Fei-Yu-Chuan-Tang (SFYCT), consisting of 13 medicinal plants, was used to treat patients with lung diseases. This study investigated the immunoregulatory effect of SFYCT on intratracheal lipopolysaccharides-(LPS-) challenged acute lung injury (ALI) mice. SFYCT attenuated pulmonary edema, macrophages, and neutrophils infiltration in the airways. SFYCT decreased inflammatory cytokines, including tumor necrosis factor-alpha (TNFalpha), interleukin-1beta, and interleukin-6 and inhibited nitric oxide (NO) production but increased anti-inflammatory cytokines, interleukin-4, and interleukin-10, in the bronchoalveolar lavage fluid of LPS-challenged mice. TNFalpha and monocyte chemotactic protein-1 mRNA expression in the lung of LPS-challenged mice as well as LPS-stimulated lung epithelial cell and macrophage were decreased by SFYCT treatment. SFYCT treatment also decreased the inducible nitric oxide synthase expression and phosphorylation of nuclear factor-kappaB (NF-kB) in the lung of mice and macrophage with LPS stimulation. SFYCT treatment dose dependency decreased the LPS-induced NO and reactive oxygen species generation in LPS-stimulated macrophage. In conclusion, SFYCT attenuated lung inflammation during LPS-induced ALI through decreasing inflammatory cytokines production while increasing anti-inflammatory cytokines production. The immunoregulatory effect of SFYCT is related to inhibiting NF-kB phosphorylation.
机译:中药式盛妃 - 川汤(SFYCT)由13种药用植物组成,用于治疗肺病患者。本研究调查了SFYCT对腹腔内脂多糖 - (LPS-)攻击急性肺损伤(ALI)小鼠的免疫调节作用。 SFYCT在气道中减弱肺水肿,巨噬细胞和中性粒细胞渗透。 SFYCT减少炎症细胞因子,包括肿瘤坏死因子-α(TNFalpha),白细胞介素-1Beta和白细胞介素-6,抑制一氧化氮(NO)生产,但在支气管饲养中增加了抗炎细胞因子,白细胞介素-4和白细胞介素-10 LPS挑战小鼠的灌洗液。通过SFYCT治疗降低了LPS攻击小鼠的肺以及LPS刺激的肺部上皮细胞和巨噬细胞的肺中TNFalpha和单核细胞趋化蛋白-1 mRNA表达。 SFYCT治疗还降低了小鼠肺肺和巨噬细胞核因子-κB(NF-KB)的诱导型一氧化氮合酶表达和磷酸化,巨噬细胞具有LPS刺激。 SFYCT治疗剂量依赖性降低了LPS刺激的巨噬细胞中的LPS诱导的NO和反应性氧物种。总之,通过降低炎性细胞因子产生的同时增加抗炎细胞因子产生,SFYCT在LPS诱导的ALI期间减弱肺炎。 SFYCT的免疫调节作用与抑制NF-KB磷酸化有关。

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