Effects of Astragaloside Ⅳ on Collagen of Myocardial Fibroblasts in Rats / 实用儿科临床杂志
Journal of Applied Clinical Pediatrics
;
(24): 553-555,558, 2007.
Artículo
en Chino
| WPRIM
| ID: wpr-641032
ABSTRACT
Objective To investigate the dose- and time-effects of astragaloside Ⅳ(XGA) on collagen of myocardial fibroblasts in rats.Methods The myocardial fibroblasts of rats were separated by collagenase and trypsinase digestive method,and the cell culture system was established. After XGA in different concentrations and at different time points was administered in fibroblast culture systems,the mRNA expression levels of collagen,matrix metalloproteinases(MMP)-1,-2,-9,tissue inhibitor of metalloproteinase(TIMP)-1 and -2 were measured with reverse transcription-polymerase chain reaction(RT-PCR) test.Results After XGA administration with different doses and at different time points was adminstered,the gel electrophoresis product of RT-PCR in fibroblast culture system expressed the mRNA of type Ⅰ,Ⅲ and Ⅳ collagens,MMP-1,-2,-9,TIMP-1 and -2;but the mRNA expression levels of type Ⅰ,Ⅲ and Ⅳ collagens,TIMP-1 and -2 decreased and the mRNA expression levels of MMP-1,-2,and -9 increased compared to those before XGA administration;the mRNA expression of type Ⅰ,Ⅲ and Ⅳ collagens,MMP-1,-2,-9,TIMP-1 and -2 decreased or increased gradually with the increase of doses and the prolonged time of XGA use.The mRNA expression levels of type Ⅰ,Ⅲ and Ⅳ collagens,TIMP-1 and -2 were negatively related to the doses and action times of XGA(r=-0.927 to -0.637 P= 0 to 0.024);and the mRNA expression levels of MMP-1,-2 and -9 were positively related to the doses and action times of XGA(r=0.672 to 0.962 P=0 to 0.034).Conclusion XGA can markedly reduce the collagen formation of myocardial fibroblasts in rats,and its mechanisms are related to the inhibiting of collagen synthesis and the increase of collagen degradation.
Texto completo:
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Índice:
WPRIM (Pacífico Occidental)
Idioma:
Chino
Revista:
Journal of Applied Clinical Pediatrics
Año:
2007
Tipo del documento:
Artículo
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