Asiatic acid ameliorates pulmonary fibrosis induced by bleomycin (BLM) via suppressing pro-fibrotic and inflammatory signaling pathways.
Idiopathic pulmonary fibrosis is known as a life-threatening disease with high mortality and limited therapeutic strategies. In addition, the molecular mechanism by which pulmonary fibrosis developed is not fully understood. Asiatic acid (AA) is a triterpenoid, isolated from Centella asiatica, exhibiting efficient anti-inflammatory and anti-oxidative activities. In our study, we attempted to explore the effect of Asiatic acid on bleomycin (BLM)-induced pulmonary fibrosis in mice. The findings indicated that pre-treatment with Asiatic acid inhibited BLM-induced lung injury and fibrosis progression in mice. Further, Asiatic acid down-regulates inflammatory cells infiltration in bronchoalveolar lavage fluid (BALF) and pro-inflammatory cytokines expression in lung tissue specimens induced by BLM. Also, Asiatic acid apparently suppressed transforming growth factor-beta 1 (TGF-β1) expression in tissues of lung, accompanied with Collagen I, Collagen III, α-SMA and matrix metalloproteinase (TIMP)-1 decreasing, as well as Smads and ERK1/2 inactivation. Of note, Asiatic acid reduces NOD-like receptor, pyrin domain containing-3 (NLRP3) inflammasome. The findings indicated that Asiatic acid might be an effective candidate for pulmonary fibrosis and inflammation treatment.
The Eastern Hospital of the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510700, China. Electronic address: dongshuhongsysu@foxmail.com.
Shu-Hong
SH
Dong
The Eastern Hospital of the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510700, China.
Yan-Wei
YW
Liu
The Eastern Hospital of the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510700, China.
Feng
F
Wei
The Eastern Hospital of the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510700, China.
Hui-Zhen
HZ
Tan
The Eastern Hospital of the First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510700, China.
Zhi-Dong
ZD
Han
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001761:Bleomycin / Q000494:pharmacology*; D001992:Bronchoalveolar Lavage Fluid / Q000166:cytology; D002460:Cell Line; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000188:drug therapy* / Q000378:metabolism; D008168:Lung / Q000187:drug effects / Q000378:metabolism; D055370:Lung Injury / Q000139:chemically induced / Q000188:drug therapy / Q000378:metabolism; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein / Q000378:metabolism; D053978:Pentacyclic Triterpenes / Q000494:pharmacology*; D011658:Pulmonary Fibrosis / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D015398:Signal Transduction / Q000187:drug effects*; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D024042:Collagen Type I; D024061:Collagen Type III; D016207:Cytokines; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D053978:Pentacyclic Triterpenes; D019715:Tissue Inhibitor of Metalloproteinase-1; D053773:Transforming Growth Factor beta1; D001761:Bleomycin; C017032:asiatic acid
Asiatic acid (AA); Bleomycin (BLM); Fibrosis; Inflammation; Pulmonary fibrosis