Impact of Toll-like receptor 4 deficiency on cerebrocardiac syndrome.
10.1007/s11596-014-1251-y
- Author:
Peng SUN
1
;
Li XU
;
Qing ZHANG
;
Qian LI
Author Information
1. Department of Emergency, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China, sp761397@sina.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Brain Ischemia;
genetics;
Electrocardiography;
Humans;
Mice;
Myocardial Reperfusion Injury;
genetics;
Myocardium;
metabolism;
pathology;
Signal Transduction;
Toll-Like Receptor 4;
biosynthesis;
deficiency;
genetics;
Tumor Necrosis Factor-alpha;
genetics
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2014;34(2):161-164
- CountryChina
- Language:English
-
Abstract:
In order to investigate the role of Toll-like receptor 4 (TLR4) in cerebrocardiac syndrome (CCS), the partial cerebral ischemia/reperfusion (I/R) models in mice with different TLR4 genotypes were established in the present study. TLR4 wild-type (C3H/HeN) and mutant (C3H/HeJ) mice of 6-8 weeks of age were divided into 4 groups at random: C3H/HeN sham group (n=10), C3H/HeJ sham group (n=10), C3H/HeN model group (n=10) and C3H/HeJ model group (n=10). Partial cerebral I/R was caused by the middle cerebral artery occlusion (MCAO) to duplicate CCS models in mice. After the operation, the electrocardiogram (ECG), the level of tumor necrosis factor-alpha (TNF-α) in myocardial tissue and the cardiac pathological changes were observed in each group. It was shown that the brain infarct volume in C3H/HeN model group was larger than that in C3H/HeJ model group (P<0.01). The ST segment change and T wave inversion occurred frequently in model groups. Moreover, the TNF-α level in C3H/HeN model group was higher than that in C3H/HeJ model group (P<0.01). The myocardial injury was aggravated in C3H/HeN group as compared with C3H/HeJ group. It was concluded that TLR4 was implicated in the development of CCS.
