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. 2011 Jul;9(3):190–206. doi: 10.2174/187152511797037583

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© 2011 Bentham Science Publishers

This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.5/), which permits unrestrictive use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Fig. (6) — Anti-ischemic treatment with ranolazine normalized the cardiac lipid metabolism and cardiac function of mice with signs of heart failure. A, B. The effect of 2 months of ranolazine treatment (Treated) on the expression of lipid metabolism genes was determined by microarray analysis of hearts isolated from 10 month-old B6 mice with 6 months of AAC (A, AAC-B6; Untreated vs. Treated), and 18 month-old ApoE^-/- mice with advanced atherosclerosis (B, ApoE^-/--18mo; Untreated vs. Treated). Gene expression is presented as fold change relative to the respective control, i.e. untreated 10 month-old sham-operated B6 mice (A, -fold of sham), and untreated 18 month-old B6 mice (B, -fold of B6); *, p<0.01. C, D. Immunohistological detection of Scd1 (upper panels), Fasn (middle panels) and Ucp1 (lower panels) was performed with the respective antibodies on heart sections of untreated (Untreated; left panels) and ranolazine-treated (Treated; right panels) 10 month-old B6 mice after 6 months of AAC (C, AACB6), and 18 month-old ApoE^-/- mice (D, ApoE^-/--18mo). Histology data are representative of at least 3 different mice/group (bar: 40 µm). Nuclei were stained with hematoxylin (upper panels). E. Cardiac triglyceride content was determined with hearts isolated from untreated (Untreated) and ranolazine- treated (Treated) 10 month-old B6 mice after 6 months of AAC (AAC-B6; left panel), and 18 month-old ApoE^-/- mice (ApoE^-/--18mo; right panel). As controls, 10 month-old, sham-operated B6 mice (Sham, left panel), and 18 month-old B6 mice (B6, right panel) were included. Data represent mean ± S. D., n=4 mice/group (**, p<0.001; *, p<0.01). F. Caspase-3 activity (Casp-3 activity) as a marker of apoptotic cell death was determined with hearts isolated from untreated (Untreated) and ranolazine-treated (Treated) 10 month-old B6 mice after 6 months of AAC (AAC-B6; left panel), and 18 month-old ApoE^-/- mice (ApoE^-/--18mo; right panel). Data are expressed as percentage of the respective control (set to 100 %), i.e. 10 month-old sham-operated B6 mice (Sham, left panel), and 18 month-old B6 mice (B6, right panel), and represent mean ± S. D., n=4 mice/group (**, p<0.001). G. The ejection fraction of untreated (Untreated) and ranolazine-treated (Treated) 10 month-old B6 mice with 6 months of AAC (AAC-B6) was determined by echocardiography. Untreated, sham-operated 10 month-old B6 mice (Sham) served as controls. Data represent mean ± S. D., n=4 mice/group (**, p<0.0005; *, p<0.01). H. The ejection fraction (expressed in %) of untreated (Untreated) and ranolazine-treated (Treated) 18 monthold ApoE^-/- mice (ApoE^-/--18mo). Untreated 18 month-old B6 mice (B6) served as controls. Data represent mean ± S. D., n=4 mice/group (**, p<0.001; *, p<0.01). I. Ranolazine-treatment (Treated; right panel) for two months did not significantly affect the atherosclerotic plaque load in the aorta of 18 month-old ApoE^-/- mice (Aorta; ApoE^-/--18mo) relative to age-matched untreated ApoE^-/- mice (Untreated; left panel).