rosmarinic-acid and Pulmonary-Fibrosis

rosmarinic-acid has been researched along with Pulmonary-Fibrosis* in 1 studies

Other Studies

1 other study(ies) available for rosmarinic-acid and Pulmonary-Fibrosis

Article	Year
Rosmarinic acid potentiates carnosic acid induced apoptosis in lung fibroblasts. PloS one, 2017, Volume: 12, Issue:9 Pulmonary fibrosis is characterized by over-population and excessive activation of fibroblasts and myofibroblasts disrupting normal lung structure and functioning. Rosemary extract rich in carnosic acid (CA) and rosmarinic acid (RA) was reported to cure bleomycin-(BLM)-induced pulmonary fibrosis. We demonstrate that CA decreased human lung fibroblast (HLF) viability with IC50 value of 17.13±1.06 μM, while RA had no cytotoxic effect. In the presence of 50 μM of RA, dose-response for CA shifted to IC50 value of 11.70±1.46 μM, indicating synergic action. TGFβ-transformed HLF, rat lung fibroblasts and L929 cells presented similar sensitivity to CA and CA+RA (20μM+100μM, respectively) treatment. Rat alveolar epithelial cells died only under CA+RA treatment, while A549 cells were not affected. Annexin V staining and DNA quantification suggested that HLF are arrested in G0/G1 cell cycle phase and undergo apoptosis. CA caused sustained activation of phospho-Akt and phospho-p38 expression and inhibition of p21 protein.Addition of RA potentiated these effects, while RA added alone had no action.Only triple combination of inhibitors (MAPK-p38, pan-caspase, PI3K/Akt/autophagy) partially attenuated apoptosis; this suggests that cytotoxicity of CA+RA treatment has a complex mechanism involving several parallel signaling pathways. The in vivo antifibrotic effect of CA and RA was compared with that of Vitamine-E in BLM-induced fibrosis model in rats. We found comparable reduction in fibrosis score by CA, RA and CA+RA, attenuation of collagen deposition and normalization of oxidative stress markers. In conclusion, antifibrotic effect of CA+RA is due to synergistic pro-apoptotic action on lung fibroblasts and myofibroblasts. Topics: Abietanes; Animals; Apoptosis; Bleomycin; Catalase; Cell Cycle; Cell Line; Cell Movement; Cell Proliferation; Cinnamates; Collagen; Depsides; Fibroblasts; Humans; Hydroxyproline; Inhibitory Concentration 50; Lipid Peroxidation; Lung; Male; Mice; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Plant Extracts; Pulmonary Alveoli; Pulmonary Fibrosis; Rats; Rats, Wistar; Rosmarinic Acid; Signal Transduction; Superoxide Dismutase; Vitamin E	2017

Article

Year

Rosmarinic acid potentiates carnosic acid induced apoptosis in lung fibroblasts.

PloS one, 2017, Volume: 12, Issue:9

Pulmonary fibrosis is characterized by over-population and excessive activation of fibroblasts and myofibroblasts disrupting normal lung structure and functioning. Rosemary extract rich in carnosic acid (CA) and rosmarinic acid (RA) was reported to cure bleomycin-(BLM)-induced pulmonary fibrosis. We demonstrate that CA decreased human lung fibroblast (HLF) viability with IC50 value of 17.13±1.06 μM, while RA had no cytotoxic effect. In the presence of 50 μM of RA, dose-response for CA shifted to IC50 value of 11.70±1.46 μM, indicating synergic action. TGFβ-transformed HLF, rat lung fibroblasts and L929 cells presented similar sensitivity to CA and CA+RA (20μM+100μM, respectively) treatment. Rat alveolar epithelial cells died only under CA+RA treatment, while A549 cells were not affected. Annexin V staining and DNA quantification suggested that HLF are arrested in G0/G1 cell cycle phase and undergo apoptosis. CA caused sustained activation of phospho-Akt and phospho-p38 expression and inhibition of p21 protein.Addition of RA potentiated these effects, while RA added alone had no action.Only triple combination of inhibitors (MAPK-p38, pan-caspase, PI3K/Akt/autophagy) partially attenuated apoptosis; this suggests that cytotoxicity of CA+RA treatment has a complex mechanism involving several parallel signaling pathways. The in vivo antifibrotic effect of CA and RA was compared with that of Vitamine-E in BLM-induced fibrosis model in rats. We found comparable reduction in fibrosis score by CA, RA and CA+RA, attenuation of collagen deposition and normalization of oxidative stress markers. In conclusion, antifibrotic effect of CA+RA is due to synergistic pro-apoptotic action on lung fibroblasts and myofibroblasts.

Topics: Abietanes; Animals; Apoptosis; Bleomycin; Catalase; Cell Cycle; Cell Line; Cell Movement; Cell Proliferation; Cinnamates; Collagen; Depsides; Fibroblasts; Humans; Hydroxyproline; Inhibitory Concentration 50; Lipid Peroxidation; Lung; Male; Mice; Oxidative Stress; p38 Mitogen-Activated Protein Kinases; Plant Extracts; Pulmonary Alveoli; Pulmonary Fibrosis; Rats; Rats, Wistar; Rosmarinic Acid; Signal Transduction; Superoxide Dismutase; Vitamin E

2017