The Influence Of Atorvastatin On Lithium Chloride Induced Expression Of Wnt/β-ca Tenin Sinaling Pathway Related Factors Of HUVECs

ObjectTO study the influence of atorvastatin for lithium chloride induced expressionof Wnt/β-catenin Signaling pathway related factors of HUVECs (Wnt1, β-catenin,dvl1) of Wnt/β-catenin signaling pathway of HUVECs, and to explore thepossible mechanisms of protecting endothelial cells.MethodsHUVECs were cultured, and were used in the experiments when they werespread and well-grown. The experiment was divided into four groups: the blankcontrol group; the activator group (final concentration of Licl was20mmol/L); theblocker group (final concentration of Licl was20mmol/L and final concentrationof rhDkk1was10ng/ml) and the atorvastatin group (final concentration of Liclwas20mmol/L and final concentration of atorvastatin was10μmmol/L). Themorphology of HUVECs were observed with inverted microscope. The functionof HUVECs were detected with nitrate reduction method. The locationalexpression of Wnt1, beta-catenin and dvl1was detected with immunohisto-chemical method in the HUVECs. The quantitative expression of Wnt1,beta-catenin and dvl1was detected with western blot method in the HUVECs.Results(1)The change of pathomorphism of HUVECs: The cells of blank controlgroup were spindle-shaped and polygonal, which showed close arrangement of monolayer pebbles; The cells of activator group shrinked, and turned round.The cells were sparse arrangement. Some cells fall off. The cells of blocker andatorvastatin group turned oval, their intercellular was narrower than the activatorgroup. A small number of cells fall off.(2)Detected the function of HUVECs with nitrate reductiontest method:Compared with the blank control group, the production of NO had significantlydecreased in the activator group, blocker group and atorvastatin group (P<0.01);Compared with the activator group, the production of NO had significantlyincreased in the blocker group and atorvastatin group (P<0.01); The blockergroup and atorvastatin group hadn,t statistical difference (P>0.05).(3)Detected the locational expression of Wnt1, beta-catenin and dvl1withimmunohistochemical method: The brown particles were observed in the cell,which showed positive expression of protein. In the cytoplasm of blank controlgroup, expression of Wnt1, beta-catenin and dvl1was very little; In the cytopl-asm of activator group, expression of Wnt1, beta-catenin and dvl1was verymuch; In the cytoplasm of blocker group and atorvastatin group, expression ofWnt1, beta-catenin and dvl1was between normal control group and activatorgroup; Compared blocker group with atorvastatin group, they weren,t difference.(4)Detected the quantitative expressions of Wnt1, beta-catenin and dvl1ofHUVECs with Western blot method: Compared with the blank control group,expressions of Wnt1, β-catenin and dvl1had significantly increased in theactivator group, group blocker and atorvastatin group (P<0.01); Compared withactivator group, expressions of Wnt1, β-catenin and dvl1had significantlydecreased in the blocker group and atorvastatin group(P<0.01); atorvastatingroup and blocker group hadn,t difference(P>0.05).Conclusions(1)The activation of Wnt/β-catenin signaling pathway had damage for the function of HUVECs, However the inhibition of this pathway had a protectiveeffect for the function of HUVECs;(2)Atorvastatin had inhibitory effect for the Wnt/β-catenin signaling path-way;(3)Atorvastatin inhibits the Wnt/β-catenin signaling pathway, which might beone of the mechanisms that could protect the function of endothelial cells.