Effect of Astragalus on Endothelin Receptor Expression in Rat Hearts with Pressure Overload-Induced Hypertrophy
WU Da-zheng
Abstract
WU Da-zheng
Abstract
OBJECTIVE To investigate the effect of Astragalus(As) on endothelin receptor(ETA,ETB) expression in left ventricular tissues in rats with pressure overload-induced cardiac hypertrophy.METHODS Cardiac hypertrophy was induced by clipping the abdominal aorta.Male SD rats were divided into six groups:sham,model,model+As-L,model+As-M,model+As-H and model+captopril(a positive control).The drugs were administered orally from the 13th week after surgery.Rats were examined after 12 weeks treatment with drugs.The cardiac hypertrophy was evaluated by Left ventricular weight index(LVWI).ETA,ETB mRNA and protein expressions in left ventricular tissues were determined by half-quantitative RT-PCR and Western blot normalized to abundance of GAPDH mRNA and protein,respectively.RESULTS The LVWI was dose-dependently inhibited by As(P0.01,P0.001).RT-PCR results demonstrated that there was no difference in the expressions of ETA or ETB mRNA among all groups.Western blot results showed that ETA and ETB protein expressions were upregulated(P0.05) significantly in model group compared with sham group.The increments of ETA,ETB protein expressions was markedly inhibited by the treatment of As-H(P0.05,P0.01).CONCLUSION As can inhibit the development of left ventricular hypertrophy in rats induced by pressure-overload and down-regulate ETA and ETB expressions in left ventricular tissues.
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OBJECTIVE To investigate the effect of Astragalus(As) on endothelin receptor(ETA,ETB) expression in left ventricular tissues in rats with pressure overload-induced cardiac hypertrophy.METHODS Cardiac hypertrophy was induced by clipping the abdominal aorta.Male SD rats were divided into six groups:sham,model,model+As-L,model+As-M,model+As-H and model+captopril(a positive control).The drugs were administered orally from the 13th week after surgery.Rats were examined after 12 weeks treatment with drugs.The cardiac hypertrophy was evaluated by Left ventricular weight index(LVWI).ETA,ETB mRNA and protein expressions in left ventricular tissues were determined by half-quantitative RT-PCR and Western blot normalized to abundance of GAPDH mRNA and protein,respectively.RESULTS The LVWI was dose-dependently inhibited by As(P0.01,P0.001).RT-PCR results demonstrated that there was no difference in the expressions of ETA or ETB mRNA among all groups.Western blot results showed that ETA and ETB protein expressions were upregulated(P0.05) significantly in model group compared with sham group.The increments of ETA,ETB protein expressions was markedly inhibited by the treatment of As-H(P0.05,P0.01).CONCLUSION As can inhibit the development of left ventricular hypertrophy in rats induced by pressure-overload and down-regulate ETA and ETB expressions in left ventricular tissues.
Key concepts: Internal medicine, Endocrinology, Endothelin receptor, Pressure overload, Endothelin 1, Muscle hypertrophy, Medicine, Left ventricular hypertrophy