Abstract
Background: Saturated fatty acids and high sugar consumption along with sedentary
lifestyle increase. The prevalence of atherosclerotic cardiovascular disease.
Objectives: In the present study, dietary high cholesterol and oxidized cholesterol
implications after myocardial infarction induced by Isoproterenol compared with
myocardial infarction subjects with normal diet were studied.
Materials and Methods: 36 animals were allocated randomly in 6 groups; three groups
were fed with standard, high-cholesterol or high-oxidized cholesterol diets for 14
weeks. The other three groups received the same diets as well as ISO to induce acute
MI. Lipid profile, OxLDL and total antioxidant levels were measured in the serum. The
myocardial CoQ10 content was analyzed using a validated RP-HPLC. The infarct size
was determined using triphenyl tetrazolium chloride staining. Histological changes and
necrosis were evaluated using microscopic analysis.
Results: Malondialdehyde concentration and infarct size in all high fat-fed groups were
increased compared to the control group, especially in the ISO-induced MI groups. The
total antioxidant level was decreased in both ISO-induced MI treated groups. CoQ10
content of the myocardium in control group (4.45 ± 0.19 μg/100 mg) was significantly
higher than cholesterol-fed (2.99 ± 0.05 μg/100mg, P < 0.001) and oxidized Cholesterolfed
(1.42 ± 0.06 μg/100mg, P = 0.00l) groups. This reduction was more intense in the
ISO-induced MI groups compared to the ISO group. High cholesterol and oxidized
cholesterol diets increased the isoproterenol-induced necrosis in the myocardium (P <
0.05, P < 0.01, respectively) compared to the rats taking normal diet.
Conclusions: Overall, we concluded that the expansion of the infarct size and reduction
of the CoQ10 content in the rat’s myocardium occurred as a result of elevated level of
high serum level of OxLDL rather than non-oxidized LDL.
lifestyle increase. The prevalence of atherosclerotic cardiovascular disease.
Objectives: In the present study, dietary high cholesterol and oxidized cholesterol
implications after myocardial infarction induced by Isoproterenol compared with
myocardial infarction subjects with normal diet were studied.
Materials and Methods: 36 animals were allocated randomly in 6 groups; three groups
were fed with standard, high-cholesterol or high-oxidized cholesterol diets for 14
weeks. The other three groups received the same diets as well as ISO to induce acute
MI. Lipid profile, OxLDL and total antioxidant levels were measured in the serum. The
myocardial CoQ10 content was analyzed using a validated RP-HPLC. The infarct size
was determined using triphenyl tetrazolium chloride staining. Histological changes and
necrosis were evaluated using microscopic analysis.
Results: Malondialdehyde concentration and infarct size in all high fat-fed groups were
increased compared to the control group, especially in the ISO-induced MI groups. The
total antioxidant level was decreased in both ISO-induced MI treated groups. CoQ10
content of the myocardium in control group (4.45 ± 0.19 μg/100 mg) was significantly
higher than cholesterol-fed (2.99 ± 0.05 μg/100mg, P < 0.001) and oxidized Cholesterolfed
(1.42 ± 0.06 μg/100mg, P = 0.00l) groups. This reduction was more intense in the
ISO-induced MI groups compared to the ISO group. High cholesterol and oxidized
cholesterol diets increased the isoproterenol-induced necrosis in the myocardium (P <
0.05, P < 0.01, respectively) compared to the rats taking normal diet.
Conclusions: Overall, we concluded that the expansion of the infarct size and reduction
of the CoQ10 content in the rat’s myocardium occurred as a result of elevated level of
high serum level of OxLDL rather than non-oxidized LDL.
Keywords
Dietary Cholesterol Myocardial Infarction Low Density Lipoprotein Rat
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Copyright
© 2018, Author(s). This open-access article is available under the Creative Commons Attribution 4.0 (CC BY 4.0) International License (https://creativecommons.org/licenses/by/4.0/), which allows for unrestricted use, distribution, and reproduction in any medium, provided that the original work is properly cited.