Fig 1: Statin rosuvastatin suppresses the apoptosis of HCAECs through regulation of the JAK2/STAT3 pathway. (A) JAK2 selective inhibitor AG490 decreased and abolished statin-regulated JAK2, p-JAK2, STAT3 and p-STAT3 expression in the HCAECs. (B) JAK2 selective inhibitor AG490 decreased and abolished statin-inhibited apoptosis of HCAECs (magnification, ×50). (C) Effects of JAK2 selective inhibitor AG490 on statin-regulated Bcl-xl and Bcl-2 protein expression in the HCAECs. (D) Effects of JAK2 selective inhibitor AG490 on statin-regulated Bax and Bad protein expression in the HCAECs. (E) Effects of JAK2 selective inhibitor AG490 on statin-regulated Bcl-xl and Bcl-2 gene expression in the HCAECs. (F) Effects of JAK2 selective inhibitor AG490 on statin-regulated Bax and Bad gene expression in HCAECs. **P<0.01; ns, not significant; HCAEC, human coronary artery endothelial cells; JAK, Janus kinase; p-, phosphorylated; STAT, signal transducer and activator of transcription.
Fig 2: Effects of surgical interventions on the expressions of regeneration-related signaling pathways.(A) Protein levels of p-STAT3 (Tyr705), STAT3, Yap, nuclear and total NF-?B p65 in regenerating liver tissue at different time points post surgery were determined by western blotting. (1, sham; 2, transection; 3, LLL resection; 4, PVL; 5, ALPPS) (B) NF-?B DNA binding activity by EMSA in the regenerating liver tissues. Five micrograms of nuclear protein were used to analyze DNA binding activity by EMSA as described in Materials and Methods. (1, sham; 2, transection; 3, LLL resection; 4, PVL; 5, ALPPS) (C) Protein levels of Yap and p-STAT3 (Tyr705) in regenerating liver tissues on day 1 after different surgical interventions were determined by IHC. (***P < 0.001 compared with the other three groups).
Fig 3: In vivo efficacy of statin rosuvastatin on myocardial infarction. (A) Statin treatment markedly decreased the mitochondrial ROS in a myocardial infarction rat model. (B) Statin treatment decreased myocardial infarction area in the experimental rats. (magnification, ×50). (C) Statin treatment decreased thrombogenesis in the experimental rats after the 60-day treatment. (D) Statin treatment decreased Bax and Bad production in the experimental rats after the 60-day treatment. (E) Statin improved the cardiac function indicators LVPWd and LVEDD. (F) Statin increased expression level of JAK and STAT3 in myocardial tissue. Scale bar, 50 µm. *P<0.05, **P<0.01. ROS, reactive oxygen species; LVPWd, left ventricular end-diastolic posterior wall thickness; LVEDD, left ventricular end-diastolic diameter; JAK, Janus kinase; STAT, signal transducer and activator of transcription.
Supplier Page from Abcam for STAT3 (pY705) + total STAT3 ELISA Kit