curcumin and Hypertrophy--Left-Ventricular

Topics: Acetylation; Animals; Blood Pressure; Curcumin; Fibrosis; Heart Failure; Hypertension; Hypertrophy, Left Ventricular; Male; Myocytes, Cardiac; Rats; Rats, Inbred Dahl; Sodium Chloride, Dietary; Stroke Volume

Background Hypertension is a cardiovascular disease which has become a major health problem in Indonesia. Left ventricle hypertrophy is one of the cardiac complications of hypertension that is characterized by thickening of the left ventricle and increasing the mass of cardiac muscle. Methods This study was an experimental study with a posttest group design. Twenty-four mice were divided into four groups. The normal group was given distilled water, the negative control group was given L-NAME 1.75 mg/25 g BW/day, the positive control group was given L-NAME 1.75 mg/25 g BW/day + captopril 0.04875 mg/30 g BW/day, and the adjuvant captopril group was given L-NAME 1.75 mg/25 g BW/day + captopril 0.04875 mg/30 g BW/day + curcuma extract 31.25 mg/30 g BW for 30 days. Results The results of one-way analysis of variance (ANOVA) test analysis on the adjuvant treatment of the captopril group revealed no significant effect on cardiac muscle mass (p > 0.05), while the thickness of the left ventricle was significant (p < 0.05). Conclusions Captopril-Curcuma group resulted in a decrease of cardiac muscle and the thickness of the left ventricle in male mice with hypertension.

Topics: Adjuvants, Pharmaceutic; Angiotensin-Converting Enzyme Inhibitors; Animals; Antioxidants; Captopril; Curcuma; Enzyme Inhibitors; Hypertension; Hypertrophy, Left Ventricular; Male; Mice; NG-Nitroarginine Methyl Ester; Plant Extracts; Treatment Outcome

The prevalence of left ventricular hypertrophy (LVH) is frequent in patients with end-stage renal disease following chronic renal failure (CRF). We investigated the therapeutic efficacy of curcumin, the principal curcuminoid of the Indian curry spice turmeric, in attenuation of LVH and sought to delineate the associated signaling pathways in blunting the hypertrophic response in nephrectomized rats. Adult Sprague-Dawley rats underwent nephrectomy (Nx) by removal of 5/6 of the kidneys. Four groups were studied for 7 wk: 1) control (sham), 2) Nx, 3) Nx + curcumin (150 mg/kg bid), and 4) Nx + enalapril (15 mg/kg bid) as positive control. Subtotal nephrectomy caused renal dysfunction, as evidenced by a gradual increase in proteinuria and elevation in blood urea nitrogen and plasma creatinine. Nx rats showed a significant hypertrophic response and increased diameter of inferior vena cava at inspiration, which was inhibited by treatment with curcumin or enalapril. Moreover, the Nx rats demonstrated changes in the signaling molecules critically involved in the hypertrophic response. These include increased glycogen synthase kinase-3β phosphorylation, β-catenin expression, calcineurin, phosphorylated (p) nuclear factor of activated T cells, pERK, and p-cAMP-dependent kinase. Both curcumin and enalapril variably but effectively deactivated these pathways. Curcumin attenuates cardiac hypertrophy and remodeling in nephrectomized rats through deactivation of multiple hypertrophic signaling pathways. Considering the safety of curcumin, these studies should facilitate future clinical trials in suppressing hypertrophy in patients with CRF.

Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Blood Pressure; Blood Urea Nitrogen; Calcineurin; Creatinine; Curcumin; Disease Models, Animal; Enalapril; Glycogen Synthase Kinase 3; Glycogen Synthase Kinase 3 beta; Hypertrophy, Left Ventricular; Kidney Failure, Chronic; Nephrectomy; NFATC Transcription Factors; Rats; Rats, Sprague-Dawley; Ventricular Remodeling