To better understand the mechanisms involved in the atherosclerosis progression, different models have been used. Currently there is no ideal model, each one has its advantages and disadvantages, especially when you want to study the disease progress. In this context we tested the hypothesis: the atherogenic “Paigen type” diet with modifications (APTDM), generates a stable model for the study of each phase of atherogenic process. Atherosclerosis was induced in 80 Wistar rats using APTDM consisting of 2 phases: 1) Hypervitamin, administered orally at a dose of 1.5 ml / kg / day for 12 days and 2) Hyperlipidic, administered for 48 days ad libitum . Experiments were carried out in 4 groups (n=16) with different doses (G1 = 75%, G2 = 50%, G3 = 33% and G4 = 25%) to obtain a dose-response curve, a healthy group (n=8; C) and a positive control (100% of the diet for 15 days; n=8; C+). Analysis was performed at day 15 for C+ and at day 30 (D30) and day 60 (D60) for the other groups. Aorta artery descending portion was extracted and histological analysis was performed to evaluate the atherosclerosis degree. Rats from C+ had severe grades (V-VII) at D15. All rats from G1 were sacrificed due to a poisoning for vitamin D2 excess. G2 rats were sacrificed at the end of D30 showing atherosclerotic lesions classified severe grades (V-VII). G3 showed mild degrees (I-III) at D30 and showed severe degrees (IV-VII) at D60. G4 showed mild degrees (I-III) at D30 and D60. Glucose, lipid profile, systolic (SBP) and diastolic (DBP) blood pressure was determined for G3. SBP decreased on D30 and D60 (123 ± 1 vs 109 ± 2 (p <0.01) and 124 ± 1 vs 99 ± 2 mmHg (p <0.01) respectively). Similar results in DBP were observed (83 ± 2 vs 69 ± 1 mmHg (p <0.01) at D60). Glucose increased on D30 and D60 (C = 98 ± 5 vs 159 ± 17 (p = 0.02) and 134 ± 4 mg/dL (p <0.01) respectively). Similar behavior for cholesterol (C = 56 ± 1 vs 114 ± 5 (p <0.01) and 128 ± 8 mg/dL (p <0.01) respectively), LDL (C = 39 ± 3 vs 103 ± 3 (p <0.01) and 123 ± 13 mg/dL (p <0.01) respectively) and triglycerides (C = 39 ± 2 vs 40 ± 1 (p = 0.01) and 74 ± 11 mg/dL (p = 0.01) respectively) was observed. HDL only increased on D60 (C = 22 ± 1 mg/dL vs 34 ± 3 (p <0.01)). In conclusion, APTDM to 33% (G3), generates a stable model for the study of the progress of each of the atherosclerosis phases in rats.
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