Effects of salviandic acid B (SA-B) on activity of basement membrane-type collagenase and impact of regulatory factors in rats with cardiac hypertrophy.
- Author:
Qi WU
1
;
Yuan PENG
;
Qianchao MENG
;
Hongyan CUI
;
Xiaoning WANG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Basement Membrane; drug effects; enzymology; Cardiomegaly; drug therapy; enzymology; genetics; Disease Models, Animal; Drugs, Chinese Herbal; pharmacology; Humans; Male; Matrix Metalloproteinase 2; genetics; metabolism; Matrix Metalloproteinase 9; genetics; metabolism; Rats; Rats, Sprague-Dawley; Tissue Inhibitor of Metalloproteinase-1; genetics; metabolism
- From: China Journal of Chinese Materia Medica 2011;36(17):2388-2392
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo observe the effect of salviandic acid B (SA-B) on MMP-2/9 and TIMP-2 of fibrotic cardiac tissues in rats and explore the action mechanism of SA-B anti-fibrosis of heart.
METHODVentricular remodeling model was induced by abdominal aortic banding (AAB) in rats. Rats were randomly divided into 6 groups: normal, model, SA-B high, SA-B middle, SA-B low and captopril control group. Histological changes of heart were observed with hemotoxylin and eosin (H&E) staining and Sirius red staining. Hydroxyproline (Hyp) content in heart tissue was measured by hydrolysis method. Expression of heart tissue collagen NIV, MMP-2/9 and TIMP-2 were analyzed with Western blot The activities of heart tissue MMP-2 were determined with gelatin zymography substrate degradation method.
RESULTSA-B treated groups had lower heart inflammation and lower heart Hyp content; decreased Collagen deposit and alleviated cardiac fibrosis. SA-B treated groups obviously decreased the expression of Collagen IV, MMP-2/9 and TIMP-2. The activity of MMP-2 was decreased in treated SA-B treated groups.
CONCLUSIONThe mechanism of SA-B action against cardiac fibrosis may be related to down-regulating the expression of TIMP -2 and the activity of MMP-2/9, thus protect the normal basal membrane.