Department of Emergency Medicine, The Second Affiliated Hospital of Soochow University, Suzhou, 215004, Jiangsu, China.
Department of Emergency Medicine, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, 221002, Jiangsu, China.
BMC Pulm Med. 2023 Sep 23;23(1):359. doi: 10.1186/s12890-023-02666-3.
The progression of acute lung injury (ALI) involves numerous pathological factors and complex mechanisms, and cause the destruction of epithelial and endothelial barriers. Pigment epithelium-derived factor (PEDF) is an angiogenesis inhibitor and a potential anti-inflammatory factor. The purpose of this study was to investigate the effect of PEDF on lipopolysaccharide (LPS)-induced ALI in rats.
In vivo, pathological and injury related factors examination were performed on rat lung to investigate the effect of PEDF on ALI. In vitro, the effect of PEDF on inflammatory injury and apoptosis of lung epithelial type II RLE-6TN cell was evaluated, and the expression of inflammatory factors and related pathway proteins and PPAR-γ (in the presence or absence of PPAR-γ inhibitors) were analyzed.
In vivo results showed that PEDF inhibited the inflammatory factor expression (TNF-α, IL-6 and IL-1β) and progression of ALI and reduced lung cell apoptosis in rats. In vitro results showed that PEDF could effectively inhibit LPS-stimulated inflammatory damage and apoptosis of RLE-6TN cells. PEDF inhibited the RLE-6TN cell injury by enhancing the expression of PPAR-γ.
PEDF is an anti-inflammatory factor, which can inhibit apoptosis of lung epithelial cells by upregulating the expression of PPAR-γ and reducing LPS-induced ALI in rats.
急性肺损伤(ALI)的进展涉及多种病理因素和复杂机制,并导致上皮和内皮屏障的破坏。色素上皮衍生因子(PEDF)是一种血管生成抑制剂和潜在的抗炎因子。本研究旨在探讨 PEDF 对脂多糖(LPS)诱导的大鼠 ALI 的影响。
在体内,通过对大鼠肺进行病理和损伤相关因素检查,研究 PEDF 对 ALI 的影响。在体外,评估 PEDF 对肺上皮细胞 II 型 RLE-6TN 细胞炎症损伤和凋亡的影响,并分析炎症因子及相关通路蛋白和 PPAR-γ(存在或不存在 PPAR-γ 抑制剂)的表达。
体内结果表明,PEDF 抑制了大鼠中炎症因子表达(TNF-α、IL-6 和 IL-1β)和 ALI 的进展,并减少了肺细胞凋亡。体外结果表明,PEDF 可有效抑制 LPS 刺激的 RLE-6TN 细胞炎症损伤和凋亡。PEDF 通过增强 PPAR-γ 的表达抑制 RLE-6TN 细胞损伤。
PEDF 是一种抗炎因子,可通过上调 PPAR-γ 的表达和减轻 LPS 诱导的大鼠 ALI 来抑制肺上皮细胞凋亡。