Journal
EUROPEAN JOURNAL OF PHARMACOLOGY
Volume 840, Issue -, Pages 9-19Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.ejphar.2018.09.030
Keywords
Pulmonary fibrosis; Inflammation; Salvianolic acid B; Endothelial permeability; Pro-inflammatory cytokine
Categories
Funding
- National Science Foundation of China [81770066, 81703117, 81470254]
- Shanghai Municipal Commission of Health and Family Planning [201640009]
- Shanghai Municipal Science and Technology Major Project [2017SHZDZX01]
- International S & T Cooperation Program of China [2013DFA30870]
- 111 Project [B13016]
- US NIH NIAID [1U01AI090909]
- China Medical Foundation (CMF)
Ask authors/readers for more resources
Endothelial cell injury and subsequent inflammation play pivotal roles in the pathogenesis of pulmonary fibrosis, a progressive and fatal disorder. We found previously that salvianolic acid B (SAB) attenuated experimental pulmonary fibrosis. Pulmonary fibrosis is driven by inflammation, but the anti-inflammatory role and mechanism of SAB on the treatment of pulmonary fibrosis is still unknown. Here, our in vivo studies showed that SAB had a strong anti-inflammatory effect on bleomycin-instilled mice by inhibiting inflammatory cell infiltration and inflammatory cytokine production. Moreover, SAB protected endothelial cells against oxidative stress injury and inhibited endothelial cell apoptosis in bleomycin-treated mice. The in vitro studies also showed that SAB decreased the H2O2-induced overproduction of reactive oxygen species to protect EA.hy926 endothelial cells from oxidative damage, and further inhibited H2O2-induced permeability and overexpression of pro-inflammatory molecules. The next studies revealed that SAB inhibited the H2O2-induced cell apoptosis and attenuated the decrease of tight junction-related gene expression, resulting in a decrease of the endothelial permeability in injured endothelial cells. Furthermore, Western blot analysis suggested that SAB decreased endothelial cell permeability and expression of pro-inflammatory cytokines by inhibiting MAPK and NF-kappa B signaling pathways. Taken together, these data indicate that SAB exerted anti-inflammatory roles in pulmonary fibrosis by protection of the endothelial cells against oxidative stress injury, mediated by inhibition of endothelial permeability and expression of pro-inflammatory cytokine via the MAPK and NF-kappa B signaling pathways.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available