3,3′,4′,5,7-Pentamethylquercetin reduces cardiac fibrosis in AngiotensinⅡ-infused rats
- VernacularTitle:五甲基槲皮素对血管紧张素Ⅱ致大鼠心肌纤维化的作用
- Author:
Zhangfan MAO
;
Zongquan SUN
;
Xinling DU
- Publication Type:Journal Article
- Keywords:
pentamethylquercetin;
AngⅡ;
cardiac fibrosis;
CVF;
NADPH oxidase
- From:
Chinese Pharmacological Bulletin
2003;0(08):-
- CountryChina
- Language:Chinese
-
Abstract:
Aim To investigate the effect of 3,3′,4′,5,7-pentamethylquercetin(PMQ) on angiotensin Ⅱ(AngⅡ) induced cardiac fibrosis.Methods Thirty rats were randomly assigned to the 5 groups,6 each:① control group: Saline was administrated daily via gavage for 21 days;② PMQ group: PMQ(50 mg?kg-1) was administrated daily via gavage for 21 days;③ AngⅡ group: AngⅡ(288 ?g?kg-1?d-1)was injected subcutaneously daily from the 15 th day;④ PMQ+ AngⅡ group: PMQ and AngⅡ were administrated as above;and ⑤ solvent+ AngⅡ group: Solvent and AngⅡ were administrated as above.After the rats were euthanized on the 22 nd day,the myocardial hydroxyproline content,SOD activity and MDA content were measured,and the expression of collagenⅠ,collagenⅢ,and NADPH oxidase subunits Nox2 and p47phox mRNA were determined by real time-PCR.Collagen volume fraction(CVF) Ⅰand Ⅲ were detected by immunohistochemistry,and CVFⅠ/CVFⅢ was calculated.Results PMQ reduced cardiac fibrosis in AngⅡ induced hypertension rats by decreasing the myocardial hydroxyproline content,downregulating the expression of collagenⅠand collagenⅢ mRNA,and decreasing CVFⅠ,CVFⅠ/CVFⅢ.PMQ exerted antioxidant function by increasing SOD activity and decreasing MDA content and reducing the mRNA expression of NADPH oxidase subunits Nox2 and p47phox.Conclusion PMQ could reduce cardiac fibrosis,which may result from the inhibition of the expression of NADPH oxidase.The results suggest that PMQ may represent a promising therapeutic approach for CHF treatment.
