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Isolation and Analysis of Plasma Lipoproteins by Ultracentrifugation
Published on: January 28, 2021
Effectiveness of Red Watermelon in Preventing Atherosclerosis Through the Role of Lipids, PCSK9, LOX-1, CD36, and
Mochamad Bahrudin1,2, Asra Al Fauzi3, Paulus Sugianto4
1Doctoral Program of Medical Science, Faculty of Medicine, Universitas Airlangga, Surabaya 60132, East Java, Indonesia.
Abstract:
Atherosclerosis is a chronic condition marked by lipid accumulation, inflammation, and endothelial dysfunction, leading to narrowed arteries and an increased risk of heart attacks and strokes. Key proteins involved in this process include PCSK9, LOX-1, ROS, CD36, and ABCA1. PCSK9 degrades LDL receptors, raising blood LDL levels, while LOX-1 and CD36 promote the uptake of oxidized LDL by macrophages, enhancing foam cell formation. ABCA1, on the other hand, facilitates cholesterol efflux to HDL, reducing atherosclerosis risk. Red watermelon (Citrullus lanatus), rich in lycopene, citrulline, and vitamins A, C, and E, has antioxidant and cardioprotective properties. This study aimed to explore the effects of red watermelon extract on the expression of PCSK9, LOX-1, ROS, TNFα, CD36, and ABCA1 in a Wistar rat model of atherosclerosis. In a randomized control trial, male Wistar rats were induced with a high-fat diet (margarine) and treated with red watermelon extract for four weeks. The findings showed that red watermelon extract reduced the expression of PCSK9, LOX-1, CD36, ROS, and TNFα, leading to lower LDL levels, and inhibited foam cell formation. It also increased ABCA1 expression, thus promoting cholesterol efflux and higher HDL levels. Path analysis confirmed that the anti-atherogenic effect of C. lanatus was primarily mediated through the PCSK9-ABCA1-FC axis. This suggests that red watermelon may serve as a natural agent for atherosclerosis prevention by regulating lipid metabolism pathways.
Insights
Red watermelon extract effectively combats atherosclerosis by lowering LDL cholesterol and reducing inflammation. It positively influences key proteins like PCSK9 and ABCA1, suggesting a natural approach to preventing heart disease.
Area of Science:
- Cardiovascular Research
- Nutraceutical Science
- Molecular Biology
Background:
- Atherosclerosis involves lipid accumulation, inflammation, and endothelial dysfunction, increasing heart attack and stroke risks.
- Key proteins like PCSK9, LOX-1, CD36, and ABCA1 play critical roles in lipid metabolism and foam cell formation.
- Red watermelon (Citrullus lanatus) possesses antioxidant and cardioprotective properties due to its rich content of lycopene, citrulline, and vitamins.
Purpose of the Study:
- To investigate the effects of red watermelon extract on atherosclerosis markers in a rat model.
- To analyze the impact of Citrullus lanatus on the expression of PCSK9, LOX-1, ROS, TNFα, CD36, and ABCA1.
- To elucidate the molecular pathways mediating the anti-atherogenic effects of red watermelon.
Main Methods:
- A randomized controlled trial using a high-fat diet-induced atherosclerosis model in Wistar rats.
- Administration of red watermelon extract to rats for four weeks.
- Measurement of protein expression levels (PCSK9, LOX-1, CD36, ABCA1, TNFα), reactive oxygen species (ROS), and lipid profiles (LDL, HDL).
- Path analysis to determine the primary mediating axis of the anti-atherogenic effect.
Main Results:
- Red watermelon extract significantly reduced the expression of PCSK9, LOX-1, CD36, ROS, and TNFα.
- The extract led to decreased LDL cholesterol levels and inhibited foam cell formation.
- ABCA1 expression was increased, promoting cholesterol efflux and elevating HDL cholesterol levels.
- Path analysis identified the PCSK9-ABCA1-FC axis as the primary mediator of Citrullus lanatus's anti-atherogenic effect.
Conclusions:
- Red watermelon extract demonstrates significant anti-atherogenic properties in a rat model.
- The extract modulates key lipid metabolism proteins, reducing LDL and increasing HDL cholesterol.
- Citrullus lanatus shows potential as a natural therapeutic agent for atherosclerosis prevention by targeting specific molecular pathways.

