Abstract: Objective To explore the effect of hydrogen sulfide (H2S) on intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of atherosclerosis in apoE knockout (apoE-/-) mice. Methods 6 week-old C57BL/6J and apoE-/- mice were divided into control C57BL/6J group, apoE-/- group, apoE-/- + sodium hydrosulfide (NaHS, a donor of H2S) group and apoE-/- + DL-propargylglycine (PPG, an inhibitor of H2S synthase). There were 8 mice in each group. They were fed chow diet for 10 weeks. Serum H2S was measured by sulfide electrode-based method, serum ICAM-1 was determined by ELISA and aortic ICAM-1 mRNA was detected by real time polymerase chain reaction. The changes of atherosclerosis plaque size were observed by oil red O staining. Results Compared with control mice, serum H2S level was significantly decreased in apoE-/- mice (P 0.01), while serum ICAM-1 and aortic ICAM-1 mRNA were markedly increased (P 0.01). The atherosclerosis plaque was obvious in apoE-/- mice. Compared with apoE-/- mice, serum H2S level was significantly increased (P 0.05), while serum ICAM-1 and aortic ICAM-1 mRNA were significantly decreased (P 0.01 and P 0.05, respectively), and the area of atherosclerosis plaque was significantly diminished (P 0.05) in apoE-/-+NaHS mice. In apoE-/-+PPG mice, serum H2S level was significantly decreased (P 0.05), while serum ICAM-1 and aortic ICAM-1 mRNA were significantly increased (P 0.05 and P 0.01, respectively), and the size of atherosclerosis plaque was significantly enlarged (P 0.01). Conclusion H2S suppressed the expression and secretion of ICAM-1 during the formation of atherosclerotic plaque.

Key words: hydrogen sulfide, atherosclerosis, Apo E knockout mice, intercellular adhesion molecule-1