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Abstract Title:

Procyanidin B2 Suppresses Lipopolysaccharides-Induced Inflammation and Apoptosis in Human Type II Alveolar Epithelial Cells and Lung Fibroblasts.

Abstract Source:

J Interferon Cytokine Res. 2019 Oct 11. Epub 2019 Oct 11. PMID: 31603717

Abstract Author(s):

Yinling Jiang, Xiaoqiong Wang, Wanchun Yang, Shuyu Gui

Article Affiliation:

Yinling Jiang

Abstract:

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.

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