【摘要】 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。Si RNA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。更多还原

【Abstract】 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 specific si RNA 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 inflammation 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 si RNA transfection, the LPS-induced inflammation and cell damage were augmented. In contrast, when H-FABP was overexpressed by pc DNA3.1-H-FABP transfection, the LPS induced inflammation and cell damage were suppressed.Conclusion: H-FABP protects cardiomyocytes from LPS-induced inflammation and cell injury.更多还原