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Macrophage scavenger receptor (SR-A I/II) deficiency reduced diet-induced atherosclerosis in C57BL/6J mice
1Pharmaceutical Technology Laboratory, Chugai Pharmaceutical Co., Ltd., Shizuoka, Japan.
Abstract:
The effects of SR-A I/II deficiency and a synthetic anti-oxidant BO-653 on a diet-induced atherosclerosis in C57BL/6J, an inbred strain known to be susceptible to diet-induced atherosclerotic lesion formation, were examined. Quantitative analysis of the extent of atherosclerotic lesions in the mice fed the high-fat diet revealed that the atherosclerotic lesion area in SR-A I/II mutants was significantly reduced by 70% compared to wild type mice. A similar level of lesion reduction (75%) was found in wild type mice fed the high-fat diet supplemented with 0.6% BO-653 compared to those without BO-653. Thus, for C57BL/6J in the setting of prolonged exposure to a high-fat diet, defect of SR-A I/II expression is significantly protective against the development of atherosclerosis, as is the synthetic anti-oxidant BO-653. These results indicate that SR-A I/II has a crucial role in atherosclerotic lesion formation with uptake of oxidized-LDL in this mouse model.
Insights
Scavenger Receptor A (SR-A) I/II deficiency significantly reduces diet-induced atherosclerosis in mice. A synthetic antioxidant, BO-653, also markedly decreased atherosclerotic lesion formation.
Area of Science:
- Cardiovascular Biology
- Atherosclerosis Research
- Pharmacology
Background:
- Diet-induced atherosclerosis is a significant health concern.
- Scavenger Receptor A (SR-A) I/II plays a role in lipid metabolism.
- Oxidized low-density lipoprotein (ox-LDL) uptake contributes to lesion development.
Purpose of the Study:
- To investigate the protective effects of SR-A I/II deficiency against diet-induced atherosclerosis.
- To evaluate the impact of the synthetic antioxidant BO-653 on atherosclerosis development.
- To elucidate the role of SR-A I/II in ox-LDL uptake in a mouse model.
Main Methods:
- Utilized C57BL/6J mice, susceptible to diet-induced atherosclerosis.
- Administered a high-fat diet to induce atherosclerotic lesion formation.
- Quantitatively analyzed atherosclerotic lesion areas in SR-A I/II deficient mice and wild-type mice with and without BO-653 supplementation.
Main Results:
- SR-A I/II deficient mice exhibited a 70% reduction in atherosclerotic lesion area compared to wild-type controls.
- Wild-type mice supplemented with 0.6% BO-653 showed a 75% reduction in lesion area.
- These findings demonstrate significant protection against atherosclerosis by both SR-A I/II deficiency and BO-653.
Conclusions:
- SR-A I/II deficiency confers significant protection against diet-induced atherosclerosis in C57BL/6J mice.
- The synthetic antioxidant BO-653 is also effective in reducing atherosclerotic lesion formation.
- SR-A I/II is crucial for atherosclerotic lesion development, likely through ox-LDL uptake.
