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Published on: October 31, 2017
[Protective effect of heart-fatty acid binding protein on lipopolysaccharide-induced cardiomyocyte damage]
Yi Li1, Kangkai Wang, Yongfang Jiang
1Department of Infectious Disease, Second Xiangya Hospital, Central South University, Changsha 410011, China.
Insights
Heart-fatty acid binding protein (H-FABP) protects heart cells from damage caused by lipopolysaccharide (LPS). Downregulating H-FABP worsens LPS-induced injury, while overexpressing it offers protection.
Area of Science:
- Cardiology
- Molecular Biology
- Cellular Biology
Background:
- Lipopolysaccharide (LPS) triggers inflammation and damage in cardiomyocytes.
- Heart-fatty acid binding protein (H-FABP) plays a role in cardiac function and injury response.
Purpose of the Study:
- To investigate the protective role of H-FABP against LPS-induced cardiomyocyte damage.
- To elucidate the molecular mechanisms underlying H-FABP's cardioprotective effects.
Main Methods:
- Primary cardiomyocyte cultures were established from neonatal rats.
- H-FABP expression was modulated using siRNA (downregulation) and pcDNA3.1-H-FABP plasmid (overexpression).
- Western blot and quantitative-PCR confirmed H-FABP expression levels. Cell viability, lactate dehydrogenase (LDH), TNF-α, and IL-1β were measured to assess cardiomyocyte injury and inflammation.
Main Results:
- LPS treatment significantly increased cardiomyocyte damage and inflammation, evidenced by decreased cell viability and elevated LDH, TNF-α, and IL-1β levels.
- Downregulation of H-FABP exacerbated LPS-induced cardiomyocyte injury and inflammation.
- Overexpression of H-FABP significantly suppressed LPS-induced inflammation and protected cardiomyocytes from damage.
Conclusions:
- H-FABP exerts a protective effect on cardiomyocytes against LPS-induced inflammation and injury.
- Modulating H-FABP expression represents a potential therapeutic strategy for managing LPS-induced cardiac 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 specific 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 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 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 LPS-induced inflammation and cell damage were suppressed.
Conclusion:
H-FABP protects cardiomyocytes from LPS-induced inflammation and cell injury.
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