Fig 2: Overexpression of CD73 improves diastolic dysfunction caused by liver cirrhosis by inhibiting the NF-kB pathway and by upregulation of A2AR expression (A) Representative high-efficiency transduction of in heart tissue. (B) Protein expression of CD73, cleaved caspase-3 and the ratio of Bax/Bcl-2 in heart tissues(n=4/group). (C) Protein expression of CD73, A2AR, IκB, p- IκB, P65 and p-P65 (n=4/group). (D) Diastolic functional indices: E/A ratio on echocardiography and LV end-diastolic pressure (LVEDP) (n=4/group). **p<0.01, ***p<0.001 vs Sham, #p<0.05, ##p<0.01 vs BDL+EMPTY. ns indicates P > 0.05, suggesting no significant difference between the indicated groups.

Fig 3: Activating A2AR meliorates cardiac inflammation and cardiomyocyte apoptosis caused by liver cirrhosis (A) Representative immunofluorescence images of TUNEL(green) (400x) in Sham, Sham+CGS 21680, BDL and BDL+ CGS 21680 group are presented. (B) Quantification results of TUNEL+ cell(n=4/group). (C) Representative images of CD45 immunohistochemistry (D) Quantification results of CD45+ cell (400x) (n=4/group). (E) Relative mRNA expression of IL-1β, il-6 and TNF-αin Sham, Sham+CGS 21680, BDL and BDL+ CGS 21680 group(n=4/group). (F) Levels of myocardium IL-1β, il-6 and TNF-αin Sham, Sham+CGS 21680, BDL and BDL+ CGS 21680 group(n=4/group). **p<0.01, ***p<0.001 vs Sham, #p<0.05, ##p<0.01, ###p<0.001 vs BDL. ns indicates P > 0.05, suggesting no significant difference between the indicated groups.