Fig. 2

Overexpression of WSB1 alleviated myocardial IR-induced injury in rats. The rats were subjected to ligation of the LAD coronary artery for 45 min and reperfusion for 6 h, 24 h or 72 h to induce IR injury, and the mRNA (A) and protein levels of WSB1 (B) in myocardial infarct penumbra area were determined by real-time PCR and western blot. The AAV9 loaded with WSB1 coding sequence was delivered into rats via intravenous injection, and IR was performed two weeks later. The WSB1 expression was verified by western blot (C) and immunohistochemistry staining (D) in penumbra myocardial tissues (the scale bar represented 50 μm). The LVEDD (E), LVESD (F), LVEF (G) and FS (H) of rats after IR for 24 h were assessed with an animal ultrasonic instrument. The CK-MB (I) and cTnI levels in serum J were determined by ELISA. K The serum LDH activity. L The infarct size of rat hearts was displayed by TTC staining. M HE staining exhibited the pathological injury in ischemic penumbra area (the scale bar represented 100 μm). (IR, ischemia–reperfusion; WSB1, WD repeat and SOCS box containing 1; LAD, left anterior descending; LVEDD left ventricular end diastolic diameter; LVESD, left ventricular systolic diameter; LVEF, left ventricular fraction; FS, fractional shortening; LDH, Lactate dehydrogenase; TTC, Triphenyltetrazolium chloride; **p < 0.01, ***p < 0.001)