Mochamad Bahrudin1,2,
Asra AI Fauzi3 
,
Paulus Sugianto4
For correspondence:- Asra Fauzi Email: asra.al@fk.unair.ac.id Tel:+6281333934999
Received: 19 March 2025 Accepted: 12 June 2025 Published: 03 July 2025
Citation: Bahrudin M, Fauzi AA, Sugianto P. Development of atherosclerotic model through margarine diet induction in Wistar rats. Trop J Pharm Res 2025; 24(6):787-793 doi: https://dx.doi.org/10.4314/tjpr.v24i6.5
© 2025 The authors.
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Purpose: To develop and analyze the relationship between dyslipidemia, inflammation, and oxidative
stress in the progression of atherosclerosis.
Methods: This study was a randomized controlled trial (RCT) on male Wistar rats (Rattus norvegicus)
induced with a high-fat diet (margarine supplementation) for 4 weeks. A total of 12 male Wistar rats
were randomly divided into control and study groups (n = 6 in each group). Control group received
standard diet for 4 weeks, while the study group received a margarine-based high-fat diet to induce
atherosclerosis over the same period. After 4 weeks, the rats were euthanized under anesthesia. Lipid
profiles (total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), triglycerides),
inflammatory biomarkers (TNF-α), oxidative stress markers (reactive oxygen species; ROS), foam cell
formation, and tunica intima thickness were assessed and compared using unpaired t-test. Regression
analysis was performed to assess the relationship between LDL and TNF-α. P < 0.05 was considered
statistically significant.
Results: The study group exhibited significantly higher levels of total cholesterol, LDL, and triglycerides,
and reduced HDL levels compared to control group (p < 0.05). Also, foam cell formation, tunica intima
thickness, ROS levels, and TNF-α ex
group. Regression analysis showed a strong positive correlation between LDL and TNF-α (r = 0.73, p <
0.05).
Conclusion: Margarine diet induces dyslipidemia and contributes to the progression of atherosclerosis.
Therapeutic interventions that target a decrease in lipid levels, as well as modulation of inflammation
and oxidative stress, may be potential targets for preventing and treating atherosclerosis
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