Icariin improves eNOS/NO pathway to prohibit the atherogenesis of apolipoprotein E-null mice.
Impaired endothelial nitric oxide synthase (eNOS)/nitric oxide (NO) pathway induces 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; lyphosphatidylcholine (LPC) group; LPC + icariin 1; LPC + icariin 3; and LPC + icariin 10. In vivo, 80 mice were separated randomly into 4 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 mass, plasma triglyceride (TG) and total cholesterol (TC) concentration, decreased aortic eNOS expression, and plasma NO concentration. LPC (10 μg/mL) treatment induced a big decline in NO level in the conditioned medium and eNOS expression, and an increase in intracellular reactive oxygen species (ROS) production in HUVECs. Icariin treatment decreased atherogenesis, ROS production, body mass, plasma TG concentration, and plasma TC concentration, and 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.
a College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, China.
Hong-Bo
HB
Xiao
a College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, China.
Guo-Guang
GG
Sui
b Hunan Province University Key Laboratory for Agricultural Biochemistry and Biotransformation, Hunan Agricultural University, Changsha 410128, China.|c Hunan Co-Innovation Center for Utilization of Botanical Functional Ingredients, Changsha 410128, China.
Xiang-Yang
XY
Lu
D000818:Animals; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics*; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism / Q000517:prevention & control*; D005419:Flavonoids / Q000494:pharmacology*; D017353:Gene Deletion; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects; D006801:Humans; D051379:Mice; D008810:Mice, Inbred C57BL; D009569:Nitric Oxide / Q000378:metabolism*; D052250:Nitric Oxide Synthase Type III / Q000235:genetics / Q000378:metabolism*
D001057:Apolipoproteins E; D005419:Flavonoids; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; C056599:icariin
atherogenesis; athérogénèse; endothelial nitric oxide synthase; icariin; icariine; nitric oxide; oxyde nitrique; oxyde nitrique synthase endothéliale