Table 1.
Oligonucleotide primers used for reverse transcription-polymerase chain reaction.
Table 2.
Effect of MHBFC on heart rate (HR) and systolic blood pressure (SBP) in different groups during the course of the experiments (, n = 6).
Table 3.
Effects of MHBFC on carotid ASBP, ADBP, AMBP and body weight in pressure-overload rats (, n = 6).
Table 4.
Effects of MHBFC on left ventricular function in pressure-overload rats (, n = 6).
Figure 1.
Representative figure of aorta remodeling in different groups.
I: Sham group; II: Model group; III: MHBFC 6 mg kg−1 group; IV: MHBFC 12 mg kg−1 group; V: Lisinopril 15 mg kg−1 group. The hypertensive vascular remodelling was observed by increases in the area of the total aorta, aorta lumen and aorta cross-sectional, which could be prevented by treatment with MHBFC at all doses for 6 weeks.
Table 5.
Effect of MHBFC on aorta remodeling in pressure-overload rats. (, n = 6).
Figure 2.
Effects of MHBFC on HW, HW/BW, LVW/BW, and RVW/BW in pressure-overload rats.
(A) Representative figure of heart macroscopic image; (B–D) statistic results. I: Sham group; II: Model group; III: MHBFC 6 mg kg−1 group; IV: MHBFC 12 mg kg−1 group; V: Lisinopril 15 mg kg−1 group. Cardiac hypertrophy was characterized by increases in the HW/BW, LVW/BW, and RVW/BW ratios, which could be reversed by MHBFC at all doses for 6 weeks. The data are expressed as the mean±SD, n = 6. #P<0.05, ##P<0.01 vs. Sham group; *P<0.05, **P<0.01 vs. Model group.
Figure 3.
Effects of MHBFC on myocyte cross-sectional area, myocardial fibrosis, perivascular fibrosis, and hydroxyproline content in cardiac tissue of pressure-overload rats.
(A) Representative figure of myocyte cross-section (HE stain, ×400); (B) statistic results of myocyte cross-section area; (C) representative figure of myocardial fibrosis (Masson’s stain, ×100); (D) statistic results of myocardial fibrosis; (E) representative figure of perivascular fibrosis (Masson’s stain, ×100); (F) statistic results of perivascular fibrosis; (G) hydroxyproline content in cardiac tissue. I: Sham group; II: Model group; III: MHBFC 6 mg kg−1 group; IV: MHBFC 12 mg kg−1 group; V: Lisinopril 15 mg kg−1 group. The myocyte cross-sectional area, levels of myocardial and perivascular fibrosis, and the hydroxyproline content all increased significantly when compared with the sham-operated rats. MHBFC at dose of 12 mg/kg for 6 weeks could reverse all these pathological changes in LVH parameters, and MHBFC at dose of 6 mg/kg for 6 weeks could reduced the myocyte cross-sectional area and level of myocardial fibrosis. The data are expressed as the mean±SD, n = 6. #P<0.05, ##P<0.01 vs. Sham group; *P<0.05, **P<0.01 vs. Model group.
Figure 4.
Effects of MHBFC on lung index (LW/BW) in pressure-overload rats.
I: Sham group; II: Model group; III: MHBFC 6 mg kg−1 group; IV: MHBFC 12 mg kg−1 group; V: Lisinopril 15 mg kg−1 group. The LW/BW ratio increased when compared with sham-operated rats, which could be completely reversed by treatment with MHBFC at all doses for 6 weeks. The data are expressed as the mean±SD, n = 6. #P<0.05, ##P<0.01 vs. Sham group; *P<0.05, **P<0.01 vs. Model group.
Figure 5.
Effects of MHBFC on atrial natriuretic peptide (ANP) mRNA expression in LV tissue of pressure-overload rats.
I: Sham group; II: Model group; III: MHBFC 6 mg kg−1 group; IV: MHBFC 12 mg kg−1 group. ANP is the molecular marker of heart failure. The ANP mRNAs were overexpressed compared with sham-operated rats, which could be completely reversed by treatment with MHBFC at all doses for 6 weeks. The data are expressed as the mean±SD, n = 3. #P<0.05, ##P<0.01 vs. Sham group; *P<0.05, **P<0.01 vs. Model group.
Figure 6.
Effects of MHBFC on plasma nitric oxide content (A), endothelial nitric oxide synthase (eNOS) protein (B and C) expression in cardiac tissue of pressure-overload rats.
I: Sham group; II:Model group; III: MHBFC 12 mg/kg group; IV: L-NAME 50 mg/kg; V: MHBFC 12 mg/kg +L-NAME 50 mg/kg; M, marker. (C) eNOS protein expression tested with immunohistology stain in interstitial tissue of myocardium and intramuscular arteries in hearts. Compared with the sham-operated rats, the plasma nitric oxide levels and the eNOS protein expression levels in the AAB-treated rat hearts decreased significantly, and this decrease could be prevented by treatment with MHBFC at 12 mg kg−1. L-NAME at 50 mg kg−1 could abolish these facilitatory effects of MHBFC. The data are expressed as the mean±SD, n = 3–6. #P<0.05, ##P<0.01 vs. Sham group; *P<0.05, **P<0.01 vs. Model group.
Figure 7.
Effects of MHBFC on plasma contents of endothelin-1(ET-1) (A), and ET-1 mRNA (B) expression in cardiac tissue of pressure-overload rats.
I: Sham group; II: Model group; III: MHBFC 12 mg kg−1 group; IV: MHBFC 6 mg kg−1 group; M, marker. The plasma contents and gene expression levels of ET-1 increased significantly 6 weeks after abdominal aortic banding. Treatment with MHBFC for 6 weeks at all doses significantly decreased the plasma contents and overexpression of ET-1 in cardiac tissue to nearly normal levels. The data are expressed as the mean±SD, n = 3–6. #P<0.05, ##P<0.01 vs. Sham group; *P<0.05, **P<0.01 vs. Model group.
Figure 8.
Effects of MHBFC on endothelin-converting enzyme (ECE) mRNA (A), endothelin receptor A (ETA) (B, immunohistology stain, ×100), and endothelin receptor B (ETB) (C, immunohistology stain, ×100) expression in cardiac tissue of pressure-overload rats.
I: Sham group; II: Model group; III: MHBFC 6 mg kg−1 group; IV: MHBFC 12 mg kg−1 group; M, marker. The gene expression levels of ECE and the cardiac tissue protein levels of ETA and ETB measured by immunohistochemistry increased significantly 6 weeks after abdominal aortic banding. Treatment with MHBFC for 6 weeks significantly decreased the overexpression of ECE genes and the increased production of ETA and ETB proteins in cardiac tissue to nearly normal levels. The data are expressed as the mean±SD, n = 3–6. #P<0.05, ##P<0.01 vs. Sham group; *P<0.05, **P<0.01 vs. Model group.