Background

Hepatic hypoxia always results in liver inflammation and dysfunction. Fatty acid-binding protein 5 (FABP5) has been reported as a hypoxia-inducible gene and a regulator of inflammatory reaction.

Objective

To evaluate the effects of FABP5 on hypoxic liver injury and its potential mechanisms.

Results

FABP5 was hypoxia-inducible expression in liver tissues and LO2 cells. The expression levels of IL6 and TNFα were upregulated with the increasing expression of FABP5 in LO2 cells. Downregulation of FABP5 expression decreased the expression levels of ALT, AST and increased cell viability of hypoxic LO2 cells. Downregulation of FABP5 expression inhibited the cyclooxygenase-2/prostaglandin E2 (COX-2/PGE2) pathway and decreased inflammatory reaction in hypoxic LO2 cells.

Conclusions

FABP5 was shown to activate COX-2/PGE2 pathway and promote hypoxic injury in LO2 cells. FABP5 may be a potential target for the treatment of hypoxic liver injury.

中文翻译：

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脂肪酸结合蛋白5激活环氧合酶2促进LO2细胞缺氧损伤

背景

肝脏缺氧总是导致肝脏炎症和功能障碍。脂肪酸结合蛋白 5 (FABP5) 已被报道为缺氧诱导基因和炎症反应的调节剂。

客观的

评估FABP5对缺氧性肝损伤的影响及其潜在机制。

结果

FABP5 在肝组织和 LO2 细胞中是缺氧诱导的表达。IL6和TNFα的表达水平随着LO2细胞中FABP5表达的增加而上调。FABP5 表达的下调降低了 ALT、AST 的表达水平，并增加了缺氧 LO2 细胞的细胞活力。FABP5 表达的下调抑制了环氧合酶-2/前列腺素 E2 (COX-2/PGE2) 通路并减少了缺氧 LO2 细胞的炎症反应。

结论

FABP5 显示激活 COX-2/PGE2 通路并促进 LO2 细胞的缺氧损伤。FABP5 可能是治疗缺氧性肝损伤的潜在靶点。