Open AccessForsythoside A protects against lipopolysaccharide-induced acute lung injury through up-regulating microRNA-124
Author(s) -
Zibin Lu,
Huayi Yang,
Hongxin Cao,
Chuying Huo,
Yuyao Chen,
Dongyi Liu,
Pei Xie,
Huixia Zhou,
Junshan Liu,
Linzhong Yu
Publication year - 2020
Publication title -
clinical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.91
H-Index - 138
eISSN - 1470-8736
pISSN - 0143-5221
DOI - 10.1042/cs20200598
Subject(s) - lipopolysaccharide , forsythia , stat3 , in vivo , inflammation , pharmacology , cytokine , lung , tumor necrosis factor alpha , infiltration (hvac) , in vitro , medicine , immunology , chemistry , signal transduction , biology , pathology , traditional chinese medicine , biochemistry , honeysuckle , alternative medicine , microbiology and biotechnology , physics , thermodynamics
Acute lung injury (ALI) is a life-threatening disease without effective pharmacotherapies, so far. Forsythia suspensa is frequently used in the treatment of lung infection in traditional Chinese medicine. In search for natural anti-inflammatory components, the activity and the underlying mechanism of Forsythoside A (FA) from Forsythia suspensa were explored. In the present paper, BALB/c mice and murine RAW 264.7 cells were stimulated by LPS to establish inflammation models. Data showed that FA inhibited the production of TNF-α and IL-6 and the activation of STAT3 in LPS-stimulated RAW 264.7 cells. Additionally, FA increased the expression level of microRNA-124 (miR-124). Furthermore, the inhibitory effect of FA on STAT3 was counteracted by the treatment of miR-124 inhibitor. Critically, FA ameliorated LPS-induced ALI pathological damage, the increase in lung water content and inflammatory cytokine, cells infiltration and activation of the STAT3 signaling pathway in BALB/c mice. Meanwhile, FA up-regulated the expression of miR-124 in lungs, while administration with miR-124 inhibitor attenuated the protective effects of FA. Our results indicated that FA alleviates LPS-induced inflammation through up-regulating miR-124 in vitro and in vivo. These findings indicate the potential of FA and miR-124 in the treatment of ALI.