Chong Lei, Liu Liu, Zhu Lili, Li Haiyan, Shao Youyou, Zhang Hailin, Yu Gang
Institute of Pediatrics, National Key Clinical Specialty of Pediatric Respiratory Medicine, The Second Affiliated Hospital of Wenzhou Medical University, Wenzhou, Zhejiang, China.
Department of Pediatrics, The Fifth Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Iran J Allergy Asthma Immunol. 2019 Feb;18(1):62-71.
Obese asthma is a new asthma phenotype. The underlying mechanisms are not clearly understood. Leptin and adiponectin are two predominant adipokines produced by adipose tissue. Studies have demonstrated a role of leptin on regulating the Janus kinase/signal transducer and ativator of transcription protein (JAK/STAT) signaling pathway and STAT3, STAT6 were known to have essential role on inflammatory cytokines production. However, whether STAT3 and STAT6 are activated and related to leptin merit further investigation. The aim of this study was to investigate the expression levels of leptin/adiponectin ratio and the activations of STAT3 and STAT6 in the lungs of obese asthma mice. Experiments were carried out on male C57/B6J mice. The proteins in bronchoalveolar lavage fluid (BALF) were measured using ELISA. The expression levels of the transcriptional and translational factors in the lungs were examined using Quantitative Reverse Transcriptase Polymerase Chain reaction (qRT-PCR) and western blot. The expression levels of leptin in the BALF of normal weight group, asthma group, obese group and obese asthma group were 2.032±0.133, 5.375±0.123, 5.418±0.165 and 7.486±0.168, respectively. The expression of leptin in obese asthma group was the highest (p<0.05) ，while the expression of adiponectin the lowest (p<0.05). The expression level of P-STAT3 in the obese asthma group was 0.9244±0.014, and was significantly higher than three other groups (p<0.05). The expressions of P-STAT6 in three other groups were all significantly higher than normal weight group (p<0.05). Our data suggest that the function of leptin on the pulmonary inflammation of obese asthma may be partly through activating the STAT3 signaling pathway.
肥胖型哮喘是一种新的哮喘表型。其潜在机制尚不清楚。瘦素和脂联素是脂肪组织产生的两种主要脂肪因子。研究表明瘦素在调节Janus激酶/信号转导子和转录激活蛋白（JAK/STAT）信号通路中发挥作用，且已知STAT3、STAT6在炎性细胞因子产生中起重要作用。然而，STAT3和STAT6是否被激活以及与瘦素的关系值得进一步研究。本研究的目的是探讨肥胖型哮喘小鼠肺组织中瘦素/脂联素比值的表达水平以及STAT3和STAT6的激活情况。实验在雄性C57/B6J小鼠上进行。使用酶联免疫吸附测定法（ELISA）检测支气管肺泡灌洗液（BALF）中的蛋白质。采用定量逆转录聚合酶链反应（qRT-PCR）和蛋白质免疫印迹法检测肺组织中转录和翻译因子的表达水平。正常体重组、哮喘组、肥胖组和肥胖型哮喘组BALF中瘦素的表达水平分别为2.032±0.133、5.375±0.123、5.418±0.165和7.486±0.168。肥胖型哮喘组中瘦素的表达最高（p<0.05），而脂联素的表达最低（p<0.05）。肥胖型哮喘组中P-STAT3的表达水平为0.9244±0.014，显著高于其他三组（p<0.05）。其他三组中P-STAT6的表达均显著高于正常体重组（p<0.05）。我们的数据表明，瘦素对肥胖型哮喘肺部炎症的作用可能部分是通过激活STAT3信号通路实现的。
