To investigate the expression changes of microRNA-19a /PI3K/AKT/PTEN pathway in rat asthma model
10.16571/j.cnki.1008-8199.2020.03.004
- VernacularTitle: microRNA-19a相关信号通路在大鼠哮喘模型中的表达变化
- Author:
Qing-hua HUANG
1
;
Lan-fang HUANG
1
;
Meng-ze LI
1
;
Chang-chun HOU
1
;
Yi-qiang CHEN
1
Author Information
1. The Institute of Respiratory Disease,the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi,China
- Publication Type:Journal Article
- Keywords:
bronchial asthma;
microRNA-19a;
AKT
- From:
Journal of Medical Postgraduates
2020;33(3):238-240
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveMiRNA can regulate the occurrence and development of many inflammatory diseases, which is one of the hot spots in the research of inflammatory diseases. Bronchial asthma is a chronic inflammation, and the role of microRNA-19a in the regulation of bronchial asthma is still unclear. This paper discusses the expression changes of microRNA-19a /PI3K/AKT/PTEN pathway in rat asthma model.Methods(1) The rat model of chronic bronchial asthma was established. (2) The expression levels of AKT, p-AKT and PTEN in lung tissues were detected by western blot. (3) microRNA-19a expression in lung tissue of the model was detected by real-time fluorescence quantitative PCR.Results(1) HE, MASSON, PSA and immunohistochemistry of lung tissues in the model were combined to determine the successful establishment of the model of chronic bronchial asthma. (2) Western blot results showed that the expression levels of AKT (0.434±0.012) and p-AKT (1.086±0.026) in asthma group were higher than those in control group and demi group. The decreased expression of PTEN (0.371±0.007) was statistically significant (P<0.05). (3)The expression of microRNA-19a in the lung tissues of the asthmatic rat model was significantly increased in the asthma group (6.22±1.61) and in the gedi group (1.93±0.54). Pair-comparison between the three groups was statistically significant (P<0.05).ConclusionThe microRNA-19a /PI3K/AKT/PTEN pathway may be involved in the pathophysiological process of bronchial asthma.
