Effect of astragaloside on TL1A expression in viral myocarditis.
10.11817/j.issn.1672-7347.2015.02.006
- Author:
Lin TIAN
1
;
Chunzhi HE
;
Shuangjie LI
Author Information
1. Department of Paediatrics, Puai Hospital, Wuhan 430000, China.
- Publication Type:Journal Article
- MeSH:
Acute Disease;
Animals;
Cardiomyopathy, Dilated;
drug therapy;
Coxsackievirus Infections;
drug therapy;
Drugs, Chinese Herbal;
pharmacology;
Mice;
Mice, Inbred BALB C;
Myocarditis;
drug therapy;
virology;
Myocardium;
metabolism;
pathology;
RNA, Messenger;
Saponins;
pharmacology;
Tumor Necrosis Factor Ligand Superfamily Member 15;
metabolism;
Up-Regulation
- From:
Journal of Central South University(Medical Sciences)
2015;40(2):150-157
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:Astragaloside is a simple substance of saponin and the active constituent of astragali. It was reported that the astragaloside exerted therapeutical eff ect on viral myocarditis and dilated cardiomyopathy. The purpose of this study was to investigate the effect of astragaloside on TL1A expression in viral myocarditis.
METHODS:A total of 100 BALB/c mice were randomly divided into 6 groups: the normal control group (group A, n=10), the high-dose control group (group B, n=10), the myocarditis control group (group C, n=20), the low-dose group (group D, n=20), the middle-dose group (group E, n=20) and the high-dose group (group F, n=20). Mice in group A and group B were injected intraperitoneally with 0.1 mL EMEM solution, while mice in group C, D, E and F were treated with 0.1 mL of 1×102 TCID50 CVB3 (diluted in EMEM). Then, mice in group A and group B were treated with carboxymethycellulose solution and 9% astragaloside for 1 week, respectively. At the same time, mice in group C, D, E and F were treated with sodium carboxymethycellulose solution, 1% [0.07 g/(kg.d)], 3% [0.2 g/(kg.d)] and 9%[0.6 g/(kg.d)] astragaloside for 1 week, respectively. After 14 days, the mice were sacrificed and their hearts were collected. The expression levels of TL1A mRNA and protein in the myocardium were examined by RT-PCR and immunohistochemistry, respectively.
RESULTS:There was no death in the group A and B. The mortality in the group C, D, E and F was 45% (9/20), 30% (6/20), 25% (5/20) and 10% (2/20), respectively. Compared with the group C, the mortality in the group F was significantly decreased (P<0.05), but there no significant difference in mortality between the group C and the group D or E (P>0.05). There was no any pathological lesion in the group A and B. The TL1A mRNA and protein expression in the myocardium of mice in the group A and B was at low level, with no difference between them (P>0.05). Compared with the group A, the expression levels of TL1A mRNA and protein in the group C were markedly up-regulated (P<0.01), which was dramatically attenuated by the intervention of astragaloside at high dosage (the group F, P<0.01) but not at low (the group D) or middle-dosage (the group E) (P>0.05).
CONCLUSION:Astragaloside may play a pivotal role in protection of the heart injury in viral myocarditis by suppressing the expression of TL1A.
