Suppression of Endoplasmic Reticulum Stress by 4-PBA Protects Against Hyperoxia-Induced Acute Lung Injury via Up-Regulating Claudin-4 Expression

• DOI: 10.3389/fimmu.2021.674316
• Publication Date: 2021-05-28T11:22:17Z
• Authors: Hsin-Ping Pao; Wen-I. Liao; Shih-En Tang; Shu-Yu Wu; Kun-Lun Huang; Shi-Jye Chu
• Keywords: Hyperoxia

Endoplasmic reticulum (ER) stress that disrupts ER function can occur in response to a wide variety of cellular factors leads the accumulation unfolded and misfolded proteins ER. Many studies have shown amplified inflammatory reactions was involved various diseases. However, little is known regarding role hyperoxia-induced acute lung injury (HALI). This study investigated influence inhibitor, 4-phenyl butyric acid (4-PBA), mice with HALI. Treatment 4-PBA hyperoxia groups significantly prolonged survival, decreased edema, reduced levels mediators, lactate dehydrogenase, protein bronchoalveolar lavage fluid, increased claudin-4 expression tissue. Moreover, stress-related expression, NF-κB activation, apoptosis In vitro study, also exerted similar effect hyperoxia-exposed mouse epithelial cells (MLE-12). when siRNA administrated MLE-12 cells, protective abrogated. These results suggested protected against ALI via enhancing expression.