Objective:To explore the effect of long non-coding RNA(lncRNA)nuclear enriched abundant transcript 1(NEAT1)on angiotensin Ⅱ(Ang Ⅱ)-induced hypertension-induced vascular remodeling by regulating the expression of miR-451a.Method:C57BL/6 mice were randomly divided into control group,model group,shR-NA group,sh-NEAT1 group,sh-NEAT1+inhibitor NC group,and sh-NEAT1+miR-451a inhibitor group,with 15 mice/group;except for the control group,the remaining mice were implanted subcutaneously with Ang Ⅱ micro-pump to establish a hypertension model,and the corresponding doses of shRNA,sh-NEAT1,inhibitor NC and miR-451a inhibitor lentiviral solution were injected into the tail vein two weeks later,respectively,while the control group and the model group were injected with equal dose of PBS.The blood pressure in mice was detected,qRT-PCR was used to detect the expression of lncRNA NEAT1 and miR-451a in thoracic aorta.HE staining and Masson staining were used to observe the histopathology of the thoracic aorta and the distribution of collagen fibers,immu-nohistochemical method was used to observe the expression of Ki-67 in thoracic aorta.Western blot was used to de-tect the expression of type Ⅰ collagen(Col1)and type Ⅲ collagen(Col3)proteins in thoracic aorta tissue,dual lucif-erase reporter gene experiment was used to verify the targeting relationship between lncRNA NEAT1 and miR-451a.Results:Compared with the control group,the systolic blood pressure(SBP),aortic tissue lncRNA NEAT1 expression,media thickness(MT)/aortic lumen diameter(LD),collagen deposition,Ki-67 positive expression,Col1 and Col3 expression in the model group were significantly increased,and the miR-451a expression was signifi-cantly decreased(P<0.05).Compared with shRNA group,the SBP,lncRNA NEAT1 expression,MT/LD,col-lagen deposition,Ki-67 positive expression,Col1 and Co13 expression in the sh-NEAT1 group were significantly re-duced,and the miR-451a expression was significantly increased(P<0.05).Compared with the sh-NEAT1+inhib-itor NC group,the SBP,MT/LD,collagen deposition,Ki-67 positive expression,Col1 and Co13 expression were significantly increased in sh-NEAT1+miR-451a inhibitor group(P<0.05).There was no significant change in ln-cRNA NEAT1 expression,the expression of miR-451a was significantly reduced(P<0.05).There was a targeting relationship between lncRNA NEAT1 and miR-451a.Conclusion:The improvement of lncRNA NEAT1 silencing on vascular remodeling in AngⅡ-induced hypertensive rats may be related to the promotion of miR-451a expression.