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Icariin improves eNOS / NO-pathway to prohibit the atherogenesis of apolipoprotein E null mice.

ABSTRACT

Impaired endothelial nitric oxide synthesis (eNOS) / nitric oxide (NO) pahtway induce the atherogenesis. The present study examined whether icariin improves the eNOS / NO pathway to prohibit the atherogenesis of apolipoprotein E-null (ApoE-/-) mice. In vitro, primary human umbilical vein endothelial cells (HUVECs) were randomly divided into 7 groups: control, vehicle; icariin 10; LPC group; LPC + icariin 1; LPC + icariin 3; LPC + icariin 10. In vivo, 80 mice were separated randomly into four groups (n = 20): control, ApoE-/- , ApoE-/- + icariin 10, and ApoE-/- + icariin 30. ApoE-/- mice had significantly more atherosclerosis in the aortic root together with increased aortic ROS production, body weight, plasma triglyceride (TG) and total cholesterol (TC) concentration, decreased aortic eNOS expression, and plasma NO concentration. LPC (10 g/ml) treatment induced a big decline in NO level in the conditioned medium and eNOS expression, an increase in intracellular reactive oxygen species (ROS) production in HUVECs. Icariin treatment decreased atherogenesis, ROS production, body weight, plasma TG concentration, and plasma TC concentration, increased NO concentration and eNOS expression. These findings suggested icariin could improve eNOS / NO-pathway to prohibit the atherogenesis of apolipoprotein E null mice by restraining oxidative stress.