a Key Laboratory of Zoonosis of Liaoning Province, College of Animal Science and Veterinary Medicine, Shenyang Agricultural University , Shenyang , Shenyang Liaoning Prov , People's Republic of China.
b Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Yantai University , Yantai , Yantai Shangdong Prov , People's Republic of China.
Pharm Biol. 2019 Dec;57(1):514-518. doi: 10.1080/13880209.2019.1648523.
ALI is a common disease characterized by acute pulmonary inflammatory disorder. Medik. (Malvaceae), as a Chinese traditional medicine, is used for the treatment of inflammation. Its main constituents are flavonoid compounds. This study investigates the regulatory effect of a TFE from leaves on gene expression in LPS-induced ALI mice via the NF-κB and MAPK signaling pathways. Kunming mice were intragastrically administered TFE (0.25, 0.5, 1.0 g/kg) for 5 days, and then ALI was induced via intranasal administration 40 μg of LPS in 10 μL PBS after intragastric administration on the 5th day, and PBS and DEX (2 mg/kg) were negative and positive control groups, respectively. The relative expression of iNOS gene was 0.707, 0.507 and 0.483 for 0.25, 0.5 and 1.0 g/kg TFE, and COX-2 gene expression was also reduced after treatment by three concentrations of TFE with 0.768, 0.545, and 0.478. The mRNA expression levels of p65 were 0.61, 0.43 and 0.27 for 0.25, 0.5 and 1.0 g/kg TFE and IκB levels were increased in a dose-dependent manner with 3.99, 13.69 and 34.36. 0.5 and 1.0 g/kg TFE inhibited the expression of ERK1/2 with 0.59 and 0.38, p38MAPK with 0.62 and 0.54, and JNK with 0.37 and 0.29, and JNK mRNA expression was 0.60 for 0.25 g/kg TFE. These results indicate that the regulatory mechanisms of TFE on gene expression in LPS-induced ALI mice include inhibition of the NF-κB and MAPK signaling pathways.
ALI 是一种常见的疾病,其特征为急性肺部炎症紊乱。药用植物(锦葵科),作为一种中药,用于治疗炎症。其主要成分是黄酮类化合物。本研究通过 NF-κB 和 MAPK 信号通路,研究了 TF 叶提取物对 LPS 诱导的 ALI 小鼠基因表达的调节作用。昆明小鼠灌胃给予 TF(0.25、0.5、1.0 g/kg),连续 5 天,第 5 天灌胃后经鼻腔给予 LPS(40 μg,10 μL PBS),建立 ALI 模型,以 PBS 和 DEX(2 mg/kg)为阴性和阳性对照组。0.25、0.5 和 1.0 g/kg TF 组 iNOS 基因的相对表达分别为 0.707、0.507 和 0.483,COX-2 基因表达也随 TF 三个浓度降低而降低,分别为 0.768、0.545 和 0.478。p65 的 mRNA 表达水平分别为 0.61、0.43 和 0.27,TF 剂量依赖性地增加 IκB 水平,分别为 3.99、13.69 和 34.36。0.5 和 1.0 g/kg TF 抑制 ERK1/2 的表达,分别为 0.59 和 0.38,p38MAPK 为 0.62 和 0.54,JNK 为 0.37 和 0.29,JNK 的 mRNA 表达为 0.60,TF 为 0.25 g/kg。这些结果表明,TF 对 LPS 诱导的 ALI 小鼠基因表达的调节机制包括抑制 NF-κB 和 MAPK 信号通路。