The protection of overexpressed β 2-AR on cadiocyte of heart failure rats and its signal pathway.

Objective:To observe the changes of the expression of the protein which concerned with cadiocyte survival during the heart failure(CCF,HF),and the mechanism of the preotection of β2-AR on cadiocyte after being transfected with Adv.β2-AR in heart failure rats.Methods:The rats model of chronic heart failure was established by partially banding abdominal aorta and the cadiocyte was isolated with collagenase II,then the cadiocyte was transfected with Adv.β2-AR to observe the change of the key proteins during the Gi-PI3K-Akt pathway in Western Blot.Results:Comparied with sham group,the overexpressed of the β2-AR protein increased the expression of phosphorylated Akt,and decreased the level of cleaved Caspase-3(p0.05).Conclusions:The overexpressed β2-AR protein can make the cadiocyte antagonist the toxic actioni of heart failure throught the Gi-PI3K-Akt pathway.