Phillygenin inhibits the inflammation and apoptosis of pulmonary epithelial cells by activating PPARγ signaling via downregulation of MMP8
Affiliations: Department of Pediatrics, Gaolangang Hospital of Zhuhai People's Hospital, Zhuhai, Guangdong 519050, P.R. China, Department of PICU, The Second Affiliated Hospital of Shandong First Medical University, Tai'an, Shandong 271000, P.R. China
- Published online on: September 6, 2021 https://doi.org/10.3892/mmr.2021.12415
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Acute lung injury (ALI) is often responsible for the high morbidity of critically ill patients. The present study aimed to investigate whether phillygenin (PHI) can inhibit inflammation and apoptosis of pulmonary epithelial cells by activating peroxisome proliferator‑activated receptor γ (PPARγ) signaling. The in vitro model of ALI was established using lipopolysaccharide (LPS) and PHI was used to treat the LPS‑induced cells. Cell viability was assessed using the MTT assay and the concentration levels of the inflammatory factors were detected by ELISA. Western blotting and reverse transcription‑quantitative PCR were conducted to measure the expression levels of the inflammation‑ and apoptosis‑associated proteins. The MMP8‑overexpression plasmid was transfected into LPS‑induced cells, which were treated with PHI treatment and the expression levels of PPARγ were detected via western blotting. PHI treatment suppressed the induction of inflammation and apoptosis of LPS‑induced BEAS‑2B cells. Furthermore, the expression levels of MMP8 in BEAS‑2B cells induced by LPS were decreased following PHI treatment. Following transfection of the MMP8 overexpression plasmid into the LPS‑induced BEAS‑2B cells and subsequent treatment of these cells with PHI, the expression levels of PPARγ were decreased. In conclusion, it was shown that PHI inhibited the inflammation and apoptosis of pulmonary epithelial cells by activating PPARγ signaling via downregulating MMP8. These data may provide valuable information for future studies exploring the therapeutic effects of PHI for ALI.