Mineralocorticoid receptors are implicated in the initial steps of the cardiorenal damage induced by ethanol

Figures

• 

  Figure 1. Role of mineralocorticoid receptors (MR) on reactive oxygen species (ROS) generation and lipoperoxidation in the left ventricle and the renal cortex of ethanol-treated rats. Serum levels of creatine phosphokinase (CK)-MB (A) and creatinine (B) were determined colorimetrically as biomarkers of cardiac and renal dysfunction, respectively. NADPH oxidase-induced superoxide (O2•−) generation was determined using the lucigenin chemiluminescence assay (C,D). The concentration of hydrogen peroxide (H2O2) was measured using a fluorogenic substrate (E,F). The levels of malondialdehyde (MDA) were determined colorimetrically as an estimative of lipoperoxidation (G,H). Control, rats receiving vehicle treatment; Ethanol, rats exposed to ethanol; MRA, rats treated with mineralocorticoid receptor antagonist; Ethanol + MRA, rats co-treated with ethanol and MRA. Results are expressed as mean ± standard error of the mean (SEM), with n = 4-7 animals per group. Statistical analysis, Two-way ANOVA followed by Tukey's post hoc test. *P < 0.05 vs. control group; ƒP < 0.05 vs. MRA and ethanol-MRA groups; #P < 0.05 vs. control and ethanol groups.

• 

  Figure 2. Enzymatic and non-enzymatic antioxidant status in the left ventricle and renal cortex of ethanol-treated rats. The activities of superoxide dismutase (SOD) (A– B), catalase (C,D), and glutathione peroxidase (GPx) (E,F) were determined colorimetrically as markers of the enzymatic antioxidant system. The concentration of reduced glutathione (GSH) (G,H) was measured as an indicator of the non-enzymatic antioxidant system. Control, rats receiving vehicle treatment; Ethanol, rats exposed to ethanol; MRA, rats treated with mineralocorticoid receptor antagonist; Ethanol + MRA, rats co-treated with ethanol and MRA. Results are expressed as mean ± standard error of the mean (SEM), with n = 4–8 animals per group. Statistical analysis, Two-way ANOVA followed by Tukey's post hoc test.

• 

  Figure 3. Role of mineralocorticoid receptors (MR) on eicosanoids production in the left ventricle and the renal cortex of ethanol-treated rats. The concentrations of thromboxane (TX)B2 (A,B), a stable metabolite of TXA2, and prostaglandin (PG)E2 (C,D) were determined by ELISA. Control, rats receiving vehicle treatment; Ethanol, rats exposed to ethanol; MRA, rats treated with mineralocorticoid receptor antagonist; Ethanol + MRA, rats co-treated with ethanol and MRA. Results are expressed as mean ± standard error of the mean (SEM), with n = 4-7 animals per group. Statistical analysis, Two-way ANOVA followed by Tukey's post hoc test. *P < 0.05 vs. control group; ƒP < 0.05 vs. MRA and ethanol-MRA groups.

• 

  Figure 4. Biomarkers of inflammation in the left ventricle and the renal cortex of ethanol-treated rats. The activities of mieloperoxidase (MPO) (A,B) and N-acetyl-beta-D-glucosaminidase (NAG) (C,D) were determined colorimetrically as an estimative of neutrophils and macrophages infiltration. The concentrations of the pro-inflammatory cytokines interleukin (IL)-6 (E,F) and IL-1β (G,H) were determined by ELISA. Control, rats receiving vehicle treatment; Ethanol, rats exposed to ethanol; MRA, rats treated with mineralocorticoid receptor antagonist; Ethanol + MRA, rats co-treated with ethanol and MRA. Results are expressed as mean ± standard error of the mean (SEM), with n = 5-8 animals per group. Statistical analysis, Two-way ANOVA followed by Tukey's post hoc test.