Key result
Luhong formula significantly lowered HW/BW, LVM/BW, and BNP levels, and inhibited myocardial fibrosis in pressure-overloaded heart failure rats.
Why the study?
Luhong formula is used to treat heart failure, but little is known about its mechanism of action.
Does Luhong formula improve left ventricular remodeling in a pressure-overloaded rat model of heart failure?
RCT (n=48)
randomly assigned
Does Luhong formula improve left ventricular remodeling in a pressure-overloaded rat model of heart failure?
Luhong formula attenuates left ventricular remodeling and myocardial fibrosis in a rat model of pressure-overload heart failure, potentially via modulation of eNOS, TGF-β1, and apoptotic pathways.
Hypothesis-generating for Luhong formula in pressure-overload remodeling; should not yet change human heart failure practice.
Background . Luhong formula (LHF)—a traditional Chinese medicine containing Cervus nippon Temminck, Carthamus tinctorius L., Astragalus membranaceus (Fisch.) Bge. var. mongholicus (Bge.) Hsiao, Codonopsis pilosula (Franch.) Nannf., Cinnamomum cassia Presl, and Lepidium apetalum Willd—is used in the treatment of heart failure, but little is known about its mechanism of action. We have investigated the effects of LHF on antifibrosis. Methods . Forty‐eight SD male rats were randomly assigned into six groups ( n = 8), model group, sham‐operation group, perindopril group (0.036 mg/ml), LHF high doses (LHF‐H, 1.44 g/mL), LHF middle doses (LHF‐M, 0.72 g/mL), and LHF low doses (LHF‐L, 0.36 g/mL). Except the sham‐operation group, the other groups were received an abdominal aorta constriction to establish a model of myocardial hypertrophy. The HW and LVW were measured to calculate the LVW/BW and HW/BW. ELISA was used to detect the serum concentration of BNP. The expressions of eNOS, TGF‐ β 1, caspase‐3, VEGF, and VEGFR2 in heart tissues were assessed by western blot analysis. mRNA expressions of eNOS, Col1a1, Col3a1, TGF‐ β 1, VEGF, and VEGFR2 in heart tissues were measured by RT‐PCR. The specimens were stained with hematoxylin‐eosin (HE) and picrosirius red staining for observing the morphological characteristics and collagen fibers I and III of the myocardium under a light microscope. Results . LHF significantly lowered the rat’s HW/BW and LVM/BW, and the level of BNP in the LHF‐treated group compared with the model group. Histopathological and pathomorphological changes of collagen fibers I and III showed that LHF inhibited myocardial fibrosis in heart failure rats. Treatment with LHF upregulated eNOS expression in heart tissue and downregulated Col1a1, Col3a1, TGF‐ β 1, caspase‐3, VEGF, and VEGFR2 expression. Conclusion . LHF can improve left ventricular remodeling in a pressure‐overloaded heart failure rat model; this cardiac protective ability may be due to cardiac fibrosis and attenuated apoptosis. Upregulated eNOS expression and downregulated Col1a1, Col3a1, TGF‐ β 1, caspase‐3, VEGF, and VEGFR2 expression may play a role in the observed LHF cardioprotective effect.
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Liu et al. (2020) conducted an RCT in myocardial hypertrophy and heart failure (n=48). Luhong formula (LHF) vs. model group, sham-operation group, and perindopril group (0.036 mg/ml) was evaluated on HW/BW, LVM/BW, and BNP levels. Luhong formula significantly lowered HW/BW, LVM/BW, and BNP levels, and inhibited myocardial fibrosis in pressure-overloaded heart failure rats.
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