Acute lung injury (ALI) is characterized by acute lung inflammation and apoptosis of alveolar epithelial cells (AECs) with a high morbidity and mortality. Procyanidin B2 (PCB2) is a naturally occurring flavonoid with anti-inflammatory activity. Our previous study demonstrated that PCB2 inhibited NLRP3 inflammasome signaling and ameliorated paraquat-induced ALI in rat, indicating the protective role of PCB2. As lipopolysaccharide (LPS) induced acute cell injury and dysfunction, we continued to evaluate the protective effects of PCB2 using LPS-treated human AECs and lung fibroblasts (LFs) model. We tested the effects of PCB2 on cell permeability, viability, apoptosis, nuclear factor-kappaB (NF-κB) activation, NLRP3 inflammasome activation, and proinflammatory cytokines production in LPS-treated human AECs and LFs. PCB2 prevented LPS-induced cell apoptosis, and increased the cell viability in LPS-treated human AECs and LFs. PCB2 inhibited LPS-induced Bax and active caspase-3 expression, and promoted Bcl-2 expression. PCB2 prevented LPS-induced tumor necrosis factor-α, interleukin-1β expression, NF-κB activation, and NLRP3 inflammasome activation. PCB2 suppressed LPS-induced inflammation and apoptosis in human AECs and LFs by inhibiting NF-κB and NLRP3 inflammasome.

中文翻译：

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原花青素 B2 在人 II 型肺泡上皮细胞和肺成纤维细胞中抑制脂多糖诱导的炎症和细胞凋亡。

急性肺损伤 (ALI) 的特征是急性肺部炎症和肺泡上皮细胞 (AEC) 的凋亡，具有高发病率和死亡率。原花青素 B2 (PCB2) 是一种天然存在的黄酮类化合物，具有抗炎活性。我们之前的研究表明，PCB2 抑制了 NLRP3 炎症小体信号传导并改善了百草枯诱导的大鼠 ALI，表明 PCB2 具有保护作用。由于脂多糖 (LPS) 诱导急性细胞损伤和功能障碍，我们继续使用 LPS 处理的人 AEC 和肺成纤维细胞 (LFs) 模型评估 PCB2 的保护作用。我们测试了 PCB2 对 LPS 处理的人类 AEC 和 LF 中细胞通透性、活力、细胞凋亡、核因子-κB (NF-κB) 激活、NLRP3 炎性体激活和促炎细胞因子产生的影响。PCB2 阻止 LPS 诱导的细胞凋亡，并增加 LPS 处理的人 AEC 和 LF 中的细胞活力。PCB2 抑制 LPS 诱导的 Bax 和活性 caspase-3 表达，并促进 Bcl-2 表达。PCB2 阻止 LPS 诱导的肿瘤坏死因子-α、白细胞介素-1β 表达、NF-κB 激活和 NLRP3 炎症小体激活。PCB2 通过抑制 NF-κB 和 NLRP3 炎症小体来抑制人 AEC 和 LF 中 LPS 诱导的炎症和细胞凋亡。