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Background: Hypercholesterolemia is a major classic risk factor for cardiovascular disease; however, there are 35%40% cases of cardiovascular where patients have normal cholesterol levels. Lp-PLA2 is an enzyme that is produced and secreted by macrophages as a response to the lipid peroxide formation, especially the platelet activating factor compound and phosphocholine peroxide. Lp-PLA2 has been correlated with classic risk factor of cardiovascular disease, although that correlation with number of foam cell at early stage of atherosclerosis is not clear yet. This study aims to determine the lipid profiles, oxidation stress markers and Lp-PLA2 levels at three different initial atherogenesis levels. Methods: This study observed the change of Lp-PLA2, F2-Isp, MDA, TC, LDL, HDL levels in rat serum at three different levels of early atherogenesis; they were Ath-I, Ath-II and Ath-III made on the number of foam cells. The number of cells was observed in all aortic cross sectional surfaces, using the Oil-Red-O staining. The LDL-C content was measured using the Fiedwall formula, whereas the MDA content was measure by using TBA-test. The observation of F2-isoprostane and Lp-PLA2 were exemplified by the procedure of Elisa’s. Results: The one way ANOVA test results between the three initial levels of atherosclerosis showed no significant differences in all lipid profiles both in serum and stress oxidation markers. However, the LSD test results projected significant differences in LDL levels in Ath-I compared to others. There was a significant difference (p<0.01) in the serum of Lp-PLA2 content. The LSD test results displayed a significant increase in Lp-PLA2 enzyme levels since the Ath-II stage. Conclussion: The elevated levels of Lp-PLA2 also increased the atherogenecity of LDL, due to the increased inflammation, stress oxidation and elevated levels of Lp-PLA2, which were interconnected with proatherogenic loops. (Indonesian J Cardiol. 2019:40:282-289)

Three Dangerous Loops Of Lipoproteine-Associated Phospholipase A2 Activity On Increasing LDL Aterogenecity