15-Lipoxygenase-2 deficiency induces foam cell formation that can be restored by salidroside through the inhibition of arachidonic acid effects DOI Creative Commons
Rong Huang, Yong Xi, Tingting Li

et al.

Open Life Sciences, Journal Year: 2025, Volume and Issue: 20(1)

Published: Jan. 1, 2025

15-Lipoxygenase-2 (15-Lox-2) is one of the key enzymes in arachidonic acid (AA) metabolic pathway, which belongs to unsaturated fatty pathway. This pathway involved foam cell transformation macrophages during progression atherosclerosis (AS). The role salidroside (SAL) cardiovascular diseases has been extensively studied, but its impact on macrophage formation not yet clearly clarified. We aimed determine effects 15-Lox-2 deficiency (Ana-1 cell) formation, and those SAL 15-Lox-2-deficient macrophages. were generated using short hairpin RNA. Results indicated that expression aorta atherosclerotic patients lower than normal group. Additionally, dramatically promoted uptake oxidized low-density lipoprotein (ox-LDL) increased Cyclin D1 level while decreasing caspase3 expression. Furthermore, inflammation, complement, TNF-α signaling pathways, along with IL1α, IL1β, IL18, Cx3cl1, activated These changes alleviated by through inhibiting AA effects, could be inhibited SAL. Consistently, phospholipase A2-inhibitor arachidonyl trifluoromethyl ketone (AACOCF3) restored these changes. In summary, reversed excessive may a promising therapeutic potential treating resulting from deficiency.

Language: Английский

15-Lipoxygenase-2 deficiency induces foam cell formation that can be restored by salidroside through the inhibition of arachidonic acid effects DOI Creative Commons
Rong Huang, Yong Xi, Tingting Li

et al.

Open Life Sciences, Journal Year: 2025, Volume and Issue: 20(1)

Published: Jan. 1, 2025

15-Lipoxygenase-2 (15-Lox-2) is one of the key enzymes in arachidonic acid (AA) metabolic pathway, which belongs to unsaturated fatty pathway. This pathway involved foam cell transformation macrophages during progression atherosclerosis (AS). The role salidroside (SAL) cardiovascular diseases has been extensively studied, but its impact on macrophage formation not yet clearly clarified. We aimed determine effects 15-Lox-2 deficiency (Ana-1 cell) formation, and those SAL 15-Lox-2-deficient macrophages. were generated using short hairpin RNA. Results indicated that expression aorta atherosclerotic patients lower than normal group. Additionally, dramatically promoted uptake oxidized low-density lipoprotein (ox-LDL) increased Cyclin D1 level while decreasing caspase3 expression. Furthermore, inflammation, complement, TNF-α signaling pathways, along with IL1α, IL1β, IL18, Cx3cl1, activated These changes alleviated by through inhibiting AA effects, could be inhibited SAL. Consistently, phospholipase A2-inhibitor arachidonyl trifluoromethyl ketone (AACOCF3) restored these changes. In summary, reversed excessive may a promising therapeutic potential treating resulting from deficiency.

Language: Английский

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