心型脂肪酸结合蛋白对脂多糖所致心肌细胞损伤的保护作用

目的：探讨心型脂肪酸结合蛋白(heart-fatt y acid binding protein，H-FABP)对脂多糖(lipopolysaccharide，LPS) 所致心肌细胞损伤的保护作用。方法：以原代培养的新生大鼠心肌细胞为模型，通过基因转染方式改变H-FABP表 达水平，采用Western印迹、定量PCR检测原代培养中H-FABP的表达。分别检测心肌细胞培养液中TNF-α，IL-1β，乳 酸脱氢酶(lactate dehydrogenase，LDH)含量以及细胞存活率来反映LPS诱导的心肌细胞损伤与炎症反应。结果：LPS处 理24 h能增加H-FABP表达。SiRNA降低H-FABP后，显著促进LPS引起的心肌细胞存活率下降、LDH释放以及TNF-α和 IL-1β释放。相反，H-FABP过表达能显著抑制LPS引起的心肌细胞损伤与炎症反应。结论：H-FABP对LPS引起的心肌 细胞损伤具有保护作用。

Protective effect of heart-fatty acid binding protein on lipopolysaccharide-induced cardiomyocyte damage

Objective: To observe the protective effect of heart-fatty acid binding protein (H-FABP) on lipopolysaccharide (LPS)-induced cardiomyocyte damage. Methods: The cardiomyocytes were isolated and cultured from 1–3 days old neonatal rats. The specifi c siRNA or plasmid of H-FABP were transfected into cells to alter H-FABP expression, which was evaluated by Western blot and quantitative-PCR. LPS-induced cardiomyocyte damage and infl ammation were estimated by detecting the contents of lactate dehydrogenase(LDH), TNF-α, and IL-1β as well as cell viability. Results: LPS treatment induced inflammation and cell damage indicated by a decrease in cell viability and an increase in LDH, TNF-α and IL-1β in the medium. When H-FABP was downregulated by siRNA transfection, the LPS-induced inflammation and cell damage were augmented. In contrast, when H-FABP was overexpressed by pcDNA3.1-H-FABP transfection, the LPSinduced inflammation and cell damage were suppressed. Conclusion: H-FABP protects cardiomyocytes from LPS-induced inflammation and cell injury.