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.

中文翻译：

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Phillygenin 通过下调 MMP8 激活 PPARγ 信号传导来抑制肺上皮细胞的炎症和凋亡。

急性肺损伤 (ALI) 通常是危重患者高发病率的原因。本研究旨在探讨 phillygenin (PHI) 是否可以通过激活过氧化物酶体增殖物激活受体 γ (PPARγ) 信号传导来抑制肺上皮细胞的炎症和凋亡。体外的使用脂多糖（LPS）建立ALI模型，并使用PHI治疗LPS诱导的细胞。使用 MTT 测定法评估细胞活力，并通过 ELISA 检测炎症因子的浓度水平。进行蛋白质印迹和逆转录定量 PCR 以测量炎症和凋亡相关蛋白的表达水平。将 MMP8 过表达质粒转染到 LPS 诱导的细胞中，用 PHI 处理，通过蛋白质印迹检测 PPARγ 的表达水平。PHI 治疗抑制了 LPS 诱导的 BEAS-2B 细胞的炎症和凋亡的诱导。此外，LPS 诱导的 BEAS-2B 细胞中 MMP8 的表达水平在 PHI 处理后降低。在将 MMP8 过表达质粒转染到 LPS 诱导的 BEAS-2B 细胞中并随后用 PHI 处理这些细胞后，PPARγ 的表达水平降低。总之，表明PHI通过下调MMP8激活PPARγ信号通路抑制肺上皮细胞的炎症和凋亡。这些数据可能为未来探索 PHI 对 ALI 的治疗效果的研究提供有价值的信息。