Baicalin attenuates LPS-induced alveolar type II epithelial cell A549 injury by attenuation of the FSTL1 signaling pathway via increasing miR-200b-3p expression

Autor: Xin-Ya Duan, Li Tao, Xun-Yan Ma, Yao-Qing Shi, Zhu-Feng Zhao, Yang Sun, Ming-Wei Liu
Jazyk: angličtina
Rok vydání: 2021
Předmět:
0301 basic medicine
Lipopolysaccharides
Follistatin-Related Proteins
MAP Kinase Signaling System
Immunology
Lung injury
FSTL1
Microbiology
03 medical and health sciences
chemistry.chemical_compound
0302 clinical medicine
Active component
medicine
Humans
Baicalin
Molecular Biology
Cell Proliferation
Flavonoids
Inflammation
Alveolar type
biology
Dose-Response Relationship
Drug
Chemistry
Epithelial Cells
Cell Biology
Original Articles
inflammatory response
RC581-607
biology.organism_classification
alveolar type II epithelial cells
Epithelium
Pulmonary Alveoli
MicroRNAs
030104 developmental biology
Infectious Diseases
medicine.anatomical_structure
miR-200b-3p
A549 Cells
030220 oncology & carcinogenesis
Cancer research
Scutellaria baicalensis
Mir 200c
Signal transduction
Inflammation Mediators
Immunologic diseases. Allergy
Signal Transduction
Zdroj: Innate Immunity, Vol 27 (2021)
Innate Immunity
ISSN: 1753-4267
1753-4259
Popis: In China, baicalin is the main active component of Scutellaria baicalensis, which has been used in the treatment of inflammation-related diseases, such as inflammation-induced acute lung injury. However, its specific mechanism remains unclear. This study examined the protective effect of baicalin on LPS-induced inflammation injury of alveolar epithelial cell line A549 and explored its protective mechanism. Compared with the LPS-induced group, the proliferation inhibition rates of alveolar type II epithelial cell line A549 intervened by different concentrations of baicalin decreased significantly, as did the levels of inflammatory factors IL-6, IL-1β, prostaglandin 2 and TNF-α in the supernatant. The expression levels of inflammatory proteins inducible NO synthase (iNOS), NF-κB65, phosphorylated ERK (p-ERK1/2), and phosphorylated c-Jun N-terminal kinase (p-JNK1) significantly decreased, as did the protein expression of follistatin-like protein 1 (FSTL1). In contrast, expression of miR-200b-3p significantly increased in a dose-dependent manner. These results suggested that baicalin could significantly inhibit the expression of inflammation-related proteins and improve LPS-induced inflammatory injury in alveolar type II epithelial cells. The mechanism may be related to the inhibition of ERK/JNK inflammatory pathway activation by increasing the expression of miR-200b-3p. Thus, FSTL1 is the regulatory target of miR-200b-3p.
Databáze: OpenAIRE
Externí odkaz: