Protective effect of heart-fatty acid binding protein on lipopolysaccharide-induced cardiomyocyte damage.
10.11817/j.issn.1672-7347.2015.05.001
- Author:
Yi LI
1
;
Kangkai WANG
;
Yongfang JIANG
;
Jun CHEN
Author Information
1. Department of Infectious Disease, Second Xiangya Hospital, Central South University, Changsha 410011, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Cell Line;
Cell Survival;
Down-Regulation;
Fatty Acid Binding Protein 3;
Fatty Acid-Binding Proteins;
metabolism;
Inflammation;
metabolism;
Interleukin-1beta;
metabolism;
L-Lactate Dehydrogenase;
metabolism;
Lipopolysaccharides;
adverse effects;
Myocytes, Cardiac;
cytology;
drug effects;
RNA, Small Interfering;
genetics;
Rats;
Transfection;
Tumor Necrosis Factor-alpha;
metabolism
- From:
Journal of Central South University(Medical Sciences)
2015;40(5):457-463
- CountryChina
- Language:Chinese
-
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 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.
