Curcumin could improve cardiac function in heart failure. - GreenMedInfo Summary
[Effects of curcumin on sarcoplasmic reticulum Ca2+-ATPase in rabbits with heart failure].
Zhonghua Xin Xue Guan Bing Za Zhi. 2010 Apr;38(4):369-73. PMID: 20654087
Department of Cardiology, Renmin Hospital of Wuhan University, Cardiovascular Research Institute, Wuhan 430060, China.
OBJECTIVE: To investigate the effects of curcumin on sarcoplasmic reticulum Ca2+-ATPase in heart failure rabbits.
METHODS: Rabbit heart failure model was made with aortic regurgitation and abdominal aorta constriction and 40 rabbits were randomly divided into 4 groups including: (1) heart failure treated with curcumin; (2) heart failure treated with placebo; (3) healthy control treated with curcumin and (4) healthy control treated with placebo. All rabbits were administrated with curcumin capsules or placebo capsules 100 mg x kg(-1) x d(-1), respectively. All groups were sacrificed after eight weeks. Myocardial ultrastructural organization was detected by transmission electron microscope. RT-PCR and Western blot were used to measure the expression of sarcoplasmic reticulum Ca2+-ATPase in mRNA and protein levels, respectively. Malachite green colorimetric assay was used to evaluate the activity of sarcoplasmic reticulum Ca2+-ATPase.
RESULTS: All detected parameters were similar between control curcumin group and control placebo group. Compared with the control groups (Groups 3 and 4), the heart/body weight ratio was significantly increased in the heart failure-curcumin group (Group 1) and the heart failure-placebo group (Group 2, all P<0.05), but the ratio was significantly lower in heart failure-curcumin group than in heart failure-placebo group (P<0.05). The degree of heart failure was decreased by curcumin. Activity and mRNA and protein expression for sarcoplasmic reticulum Ca2+-ATPase were significantly reduced in the heart failure-placebo group and which could be significantly attenuated by curcumin (all P<0.05).
CONCLUSION: Curcumin could improve cardiac function via upregulating the expression of sarcoplasmic reticulum Ca2+-ATPas in this model.