Fig 2: HRS suppressed myocardial cell apoptosis via the PI3K/Akt signaling pathway. (A) Western blot assays were performed. The levels of (B) p-Akt, (C) HO-1, (D) PI3K and (E) Akt were quantified. Data among multiple groups were compared using one-way analysis of variance. *P<0.05 vs. CPB group; #P<0.05 vs. PI3K group. PI3K group, LY294002 + CPB; LHRS group, LY294002 + CPB + HRS; CPB, cardiopulmonary bypass; HRS, hydrogen rich solution; PI3K, phosphatidylinositol 3-kinase; Akt, proein kinase B; p-, phosphrylated; HO-1, heme oxygenase 1.

Fig 3: KOR agonist activates PI3K/AKT-related proteins to inhibit neuronal apoptosis in CPB rats. (A) Inflammatory factors detected by ELISA. (B) Western blot were used to detect apoptosis factors of Bax and Bcl-2. (C) TUNEL staining (scale bar, 50 µm). (D) Expression levels of PI3K/AKT-related proteins were detected by western blotting. n=10; *P<0.05. KOR, ?-opioid receptor; CPB, cardiopulmonary bypass; p-, phosphorylated.

Fig 4: RBM24 promotes chemotherapeutic drug-induced apoptosis of CRC cells. (A, B) The apoptosis rate of RBM24-overexpressing HCT116 cells that were untreated or treated with 2 µg/ml of 5-FU or 1 µg/ml of DDP. (B) Quantification. (C, D) The apoptosis rate of RBM24-overexpressing SW480 cells untreated, or treated with 2 µg/ml of 5-FU or 1 µg/ml of DDP. (D) Statistical analysis. (E, F) The apoptosis rate of RBM24-overexpressing LoVo cells that were untreated or treated with 2 µg/ml of 5-FU or 1 µg/ml of DDP. (F) Quantification. (G) The apoptosis rate of RBM24-overexpressing HCT116 cells following treatment with 1 µM of SF1670 for 48 h. (H, I) SF1670 treatment (1 µM) for 48 h decreased the sensitivity of RBM24-overexpressing HCT116 cells to 5-FU or DDP, as compared with the cells treated with 5-FU or DDP for 48 h alone. (J) The protein levels of cleaved Caspase3 and cleaved PARP, the phosphorylation levels of Akt, ATR, ATM and H2AX were analysed by Western blotting analysis in RBM24-overexpressing HCT116 cells that were co-treated with SF1670 and 5-FU/DDP for 48 h. Data were analysed by two-tailed Student's t-test. Multiple comparisons were performed using one-way ANOVA with post hoc LSD test. Error bars represented as S.D from at least three independent experiments. *p<.05, **p<.01. 5-FU, 5-fluorouracil; DDP, cis-diamminedichloroplatinum

Fig 5: URRCC is associated with EGFL7/P-AKT/FOXO3 signaling pathway. a and b: WB analysis of T-AKT, P-AKT, and FOXO3 in URRCC-overexpressing or URRCC-inhibited A498 and OSRC-2 cells compared with sh-control or mock group, ß-actin was used as a loading control. c: CCK8 assays of A498 cells transfected with mock/oe-URRCC and si-NC/si-EGFL7. d: Representative images and the numbers of invasive cells per high-power field reduced after the transfection with mock/oe-URRCC and si-NC/si-EGFL7 in A498 cells. e: WB analysis for EGFL7, T-AKT, P-AKT, and FOXO3 protein levels of A498 cells transfected with mock/oe-URRCC and si-NC/si-EGFL7. ß-actin was used as a loading control