Total flavonoids of bugloss limits left ventricular remodeling after myocardial infarction in mice
- Author:
Shou-Bao WANG
1
,
2
;
Dan-Shu WANG
;
Yi-Huang LIN
;
Rong-Rong WANG
;
Lian-Hua FANG
;
Yang LYU
;
Guan-Hua DU
Author Information
1. Beijing Key Laboratory of Drug Targets Identification and Drug Screening
2. State Key Laboratory of Bioactive Substance and Function of Natural Medicines
- Keywords:
total flavonoids of bugloss;
myocardial infarction;
left ventricular remodeling;
hypertrophy
- From:
Chinese Journal of Pharmacology and Toxicology
2018;32(4):306-306
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To investigate the effects of total flavonoids of bugloss(TFB)on left ventricular (LV)remodeling after myocardial infarction(MI),LV size and function was compared in mice subjected to left anterior descending coronary artery ligation. METHODS 28 d after MI, the infarcted fraction of the LV and LV mass, systolic and diastolic function were measured. Capillary density and myocyte width in the nonischemic portion of the LV were also determined.RESULTS 28 d after MI,both groups had dilated LVs with decreased fractional shortening and lower ejection fractions. Although the infarcted size of the LV was similar in both groups,LV end-diastolic internal diameter,end-diastolic volume,and mass were lower, but fractional shortening, ejection fraction, and the maximum rate of developed LV pressure(dp/dtmax)were greater in TFB treated mice than in control mice.Impairment of diastolic func-tion, as measured by the time constant of isovolumic relaxation (t) and the maximum rate of LV pres-sure decay(dp/dtmin),was more marked in control mice than in TFB treated mice.Mortality after MI was greater in control mice than in TFB treated mice.In control mice,capillary density and myocyte width in the nonischemic portion of the LV did not differ before and 28 days after MI, whereas in TFB treated mice, capillary density increased and myocyte width declined after MI. CONCLUSION These results suggest that the presence of TFB limits LV dysfunction and remodeling in a murine model of MI in part by decreasing myocyte hypertrophy in the remote myocardium.
