[Expression of Toll-like receptor 2/4 mRNA in myocardium in mice with hemorrhagic shock].
OBJECTIVE
To investigate the effect of hemorrhagic shock without resuscitation on expression of Toll-like receptor (TLR) in myocardium of rats and its significance.


METHODS
Forty-five C57BL/6 mice were randomly divided into 3 groups: hemorrhagic group, sham operation group and lipopolysaccharide (LPS) group, with 15 mice in each group. The hemorrhagic shock mouse model was reproduced by heart puncture. Expression levels of TLR2 mRNA and TLR4 mRNA were determined by reverse transcription-polymerase chain reaction (RT-PCR). Left ventricular end-systolic pressure (LVESP) was determined and adopted as an index of left ventricle contractile function.


RESULTS
(1)Both hemorrhagic shock and LPS challenge led to a reduction in arterial blood pressure in mice when compared with sham operation group. Both hemorrhagic shock and LPS challenge could result in left ventricle contractile dysfunction when compared with sham operation group. (2)Expression levels for TLR2 and TLR4 genes were upregulated in myocardium to various extents after hemorrhagic shock and LPS challenge, while in contrast the changes were absent in sham operation group.


CONCLUSIONS
(1)The up-regulation of TLR2 and TLR4 genes is closely related with hemorrhagic shock and LPS-induced left ventricle contractile dysfunction, and there may exist a difference in signal transduction pathway between the two pathological conditions. (2)The host ability of innate immune response may be reinforced by the up-regulation of TLR2 and TLR4, whereas overexpression of them may also impair the function of tissues or organs.
Hang
Tao
T
Department of Cardiology, Nanjing General Hospital of Nanjing Command, Nanjing 210002, Jiangsu, China. njht1976@yahoo.com.cn
Jiang
Shi-sen
SS
Gong
Jian-bin
JB
Lü
Tang-feng
TF
Song
Yong
Y
Zhuge
Hai-hong
HH
D000818:Animals; D006352:Heart Ventricles / Q000503:physiopathology; D008070:Lipopolysaccharides / Q000494:pharmacology; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism*; D012333:RNA, Messenger / Q000096:biosynthesis; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012771:Shock, Hemorrhagic / Q000503:physiopathology*; D015398:Signal Transduction; D051195:Toll-Like Receptor 2 / Q000096:biosynthesis* / Q000235:genetics; D051197:Toll-Like Receptor 4 / Q000096:biosynthesis* / Q000235:genetics; D015854:Up-Regulation
D008070:Lipopolysaccharides; D012333:RNA, Messenger; D051195:Toll-Like Receptor 2; D051197:Toll-Like Receptor 4