Chlorogenic Acid Inhibited Epithelial-Mesenchymal Transition to Treat Pulmonary Fibrosis through Modulating Autophagy

Area of Science:

• Pharmacology
• Cell Biology
• Respiratory Medicine

Background:

• Pulmonary fibrosis (PF) is a chronic lung disease with limited treatment options.
• Chlorogenic acid (CGA) exhibits anti-inflammatory and antioxidant properties.
• The precise mechanism of CGA in treating PF, particularly its effects on epithelial-mesenchymal transition (EMT) and autophagy, requires elucidation.

Purpose of the Study:

• To investigate the therapeutic mechanism of CGA in a mouse model of bleomycin (BLM)-induced PF.
• To evaluate the effects of CGA on EMT and autophagy in both in vivo and in vitro models.
• To confirm whether CGA's inhibition of EMT is mediated by autophagy activation.

Main Methods:

• In vivo study: BLM-induced PF mice treated with CGA (60 mg/kg).
• In vitro study: TGF-β1-induced EMT cell model treated with CGA (50 µM).
• Verification: Use of autophagy inhibitor (3-methyladenine) to assess CGA's mechanism.

Main Results:

• CGA treatment significantly reduced lung inflammation and fibrosis in BLM-induced PF mice.
• CGA inhibited EMT and promoted autophagy in PF mice.
• In vitro, CGA inhibited TGF-β1-induced EMT and upregulated autophagy markers; this effect was reversed by an autophagy inhibitor.

Conclusions:

• Chlorogenic acid demonstrates therapeutic potential for pulmonary fibrosis.
• CGA exerts its protective effects by inhibiting epithelial-mesenchymal transition through the activation of autophagy.
• These findings highlight CGA as a promising agent for PF treatment via modulation of autophagy and EMT.