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Hydrogen sulfide (H 2 S) exerts an anti‑atherosclerotic effect and decreases foam cell formation. Lipoprotein‑associated phospholipase A2 (Lp‑PLA 2 ) is a key factor involved in foam cell formation. However, the association between H 2 S and Lp‑PLA 2 expression levels with respect to foam cell formation has not yet been elucidated. The present study investigated whether H 2 S can affect foam cell formation and potential signalling pathways via regulation of the expression and activity of Lp‑PLA 2 . Using human monocytic THP‑1 cells as a model system, it was observed that oxidized low‑density lipoprotein (ox‑LDL) not only upregulates the expression level and activity of Lp‑PLA 2 , it also downregulates the expression level and activity of Cystathionine γ lyase. Exogenous supplementation of H 2 S decreased the expression and activity of Lp‑PLA 2 induced by ox‑LDL. Moreover, ox‑LDL induced the expression level and activity of Lp‑PLA 2 via activation of the p38MAPK signalling pathway. H 2 S blocked the expression levels and activity of Lp‑PLA 2 induced by ox‑LDL via inhibition of the p38MAPK signalling pathway. Furthermore, H 2 S inhibited Lp‑PLA 2 activity by blocking the p38MAPK signaling pathway and significantly decreased lipid accumulation in ox‑LDL‑induced macrophages, as detected by Oil Red O staining. The results of the present study indicated that H 2 S inhibited ox‑LDL‑induced Lp‑PLA 2 expression levels and activity by blocking the p38MAPK signalling pathway, thereby improving foam cell formation. These findings may provide novel insights into the role of H 2 S intervention in the progression of atherosclerosis.

Hydrogen sulfide improves ox‑LDL‑induced expression levels of Lp‑PLA2 in THP‑1 monocytes via the p38MAPK pathway

Hydrogen sulfide improves ox‑LDL‑induced expression levels of Lp‑PLA₂ in THP‑1 monocytes via the p38MAPK pathway