Feifukang ameliorates pulmonary fibrosis by inhibiting JAK-STAT signaling pathway

  title={Feifukang ameliorates pulmonary fibrosis by inhibiting JAK-STAT signaling pathway},
  author={Hongbo Li and Zhenkai Wang and Jie Zhang and Youlei Wang and Chen Yu and Jinjin Zhang and Xiaodong Song and Changjun Lv},
  journal={BMC Complementary and Alternative Medicine},
BackgroundFeifukang (FFK) is a traditional Chinese medicine composed of herbs that protect lung function. However, difficulty arises regarding the clinical application of FFK due to the complex mechanism of Chinese medicines. This study aimed to investigate the efficacy of FFK and explore its targeted genes and pathways.MethodsHistopathological changes and collagen deposition were measured to evaluate the effect of FFK on bleomycin-induced pulmonary fibrosis in mice. The differentially… 
The role of natural products in the prevention and treatment of pulmonary fibrosis: a review.
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Natural Product-Based Potential Therapeutic Interventions of Pulmonary Fibrosis
The signaling mechanisms of PF pathogenesis, the potential opportunities offered by natural product-based medicine in treating PF, and the potential uses of natural products are revealed.
Clinical efficacy of Chinese herbs for supplementing qi and activating blood circulation combined with N-acetylcysteine in the treatment of idiopathic pulmonary fibrosis: A systematic review and network meta-analysis
CH related treatments may have advantages in the treatment of IPF and CH + NAC may have clinical application value, however, limited by the quality and quantity of researches included, more rational and scientific randomized controlled trials containing large sample sizes need to be conducted to further verify the conclusions.
The Roles of Immune Cells in the Pathogenesis of Fibrosis
Recent advances in understanding the roles of immune cells in regulating fibrotic development and immune-based therapies in different disorders are summarized and the underlying molecular mechanisms with a focus on mTOR and JAK-STAT signaling pathways are discussed.
Novel Pyrimidines as Multitarget Protein Tyrosine Kinase Inhibitors for the Treatment of Idiopathic Pulmonary Fibrosis (IPF)
Investigating a new class of pyrimidine derivatives identified as potent protein tyrosine kinase (PTK) inhibitors for the treatment of idiopathic pulmonary fibrosis suggested that the multi‐PTK inhibitor 6 a may serve as a promising agent for the Treatment of IPF.


Protective roles of pulmonary rehabilitation mixture in experimental pulmonary fibrosis in vitro and in vivo
  • L. Zhang, Y. Ji, W. Jiang, C. Lv
  • Medicine, Biology
    Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
  • 2015
In this study, PRM prevented experimental pulmonary fibrosis by modulating the HMGB1/RAGE pathway and significantly decreased EMT and preventedmonary fibrosis through decreasingHMGB1 and regulating RAGE in vitro and in vivo.
Formononetin Inhibited the Inflammation of LPS-Induced Acute Lung Injury in Mice Associated with Induction of PPAR Gamma Expression
Treatment with the formononetin group markedly attenuated inflammatory cell numbers in the BALF, increased PPAR-γ gene expression and improved SOD activity and inhibited MPO activity, and showed a protective effect on LPS-induced acute lung injury in mice.
Dexamethasone attenuates bleomycin-induced lung fibrosis in mice through TGF-β, Smad3 and JAK-STAT pathway.
It was found that BLM promoted the development of inflammation, leading to severe pulmonary fibrosis with the increasing of TGF-β1, Smad3 and STAT1, and there is a possible pathway of mousemonary fibrosis model through T GF-β, SmAD3 and JAK-STAT pathway.
mTOR Overactivation and Compromised Autophagy in the Pathogenesis of Pulmonary Fibrosis
It is concluded that mTOR overactivation in AECs and compromised autophagy in the lungs are involved in the pathogenesis of pulmonary fibrosis and the suppression of mTOR and enhancement of Autophagy may be used for treatment of pulmonary Fibrosis.
Efficacy and safety of nintedanib in idiopathic pulmonary fibrosis.
In patients with idiopathic pulmonary fibrosis, nintedanib reduced the decline in FVC, which is consistent with a slowing of disease progression; nintinganib was frequently associated with diarrhea, which led to discontinuation of the study medication in less than 5% of patients.
Protective effect of polyphenols in an inflammatory process associated with experimental pulmonary fibrosis in mice
The findings confirmed the anti-inflammatory effects of resveratrol and quercetin in BLM-induced lung damage, and highlight, for the first time, the protective properties of exogenous administration of mangiferin and DHQ on experimental pulmonary fibrosis.
Astaxanthin prevents pulmonary fibrosis by promoting myofibroblast apoptosis dependent on Drp1-mediated mitochondrial fission
Astaxanthin can prevent pulmonary fibrosis by promoting myofibroblast apoptosis through a Drp1‐dependent molecular pathway and provides a potential therapeutic value in pulmonary fibrotic treatment.
Pharmacodynamic and pharmacokinetic assessment of pulmonary rehabilitation mixture for the treatment of pulmonary fibrosis
PRM exhibited a satisfactory pharmacodynamic and pharmacokinetic performance, which highlights PRM as a potential multi-target oral drug for the treatment of pulmonary fibrosis.