Fig 1: H/R treatment promotes cardiomyocyte apoptosis and downregulates KDM1A.HL-1 cells were subjected to hypoxia-reoxygenation treatment (the H/R group), with HL-1 cells untreated as the control (the Blank group). (A–B) qRT-PCR and Western blot were adopted to detect the levels of KDM1A in HL-1 cells; (C) CCK-8 was used to verify HL-1 cell viability; (D) ELISA was performed to detect the concentrations of myocardial injury markers in HL-1 cells; (E) qRT-PCR was used to detect the mRNA levels of apoptotic proteins in HL-1 cells; (F) Flow cytometry was conducted to detect the apoptosis rate of HL-1 cells; (G) Colorimetric method was used to examine the activities of Caspase-3 and Caspase-9. The cell experiment was repeated three times independently; data were expressed as mean ± standard deviation. Data in (A–B) and (D–G) were tested by independent t test; data in (C) were analyzed by two-way ANOVA, followed by Tukey’s post-hoc test. LDH, Lactate Dehydrogenase; AST, Aspartate Aminotransferase; CK-MB, Creatine Kinase-MB.
Fig 2: Validation of liver cirrhosis model.(A, B) HE and Masson staining between the normal group and the LC group (n = 6); (C–E) Changes in the levels of the serological indicators ALT, AST, and ALP in the normal and LC groups (n = 6); Scale bar (A, B) 50 µm. All data are shown as the means ± SD (Student’s t, n = 3). *P < 0.05, **P < 0.01, ***P < 0.001.
Fig 3: AKR1B10 expression is highly expressed in the liver tissues of AH mice.A Volcano map of the gene expression obtained from the GSE28619. The│logFC│ > 0 indicates an upregulated gene; │logFC│ < 0 indicates downregulated gene. Red dots represent the significantly upregulated genes; green points represent the significantly downregulated genes. B, Boxplot of AKR1B10 mRNA expression in microarray GSE28619. The left blue box shows the expression of the normal samples (n = 7); the right red box shows the expression of AH patient samples (n = 15). C, D Serum levels of ALT, AST, TNF-α, and IL-6 as ELISA detected. E Liver damage in liver tissues of AH mice as H&E staining measured (400×). F Lipid drops in liver tissues of AH mice by oil red O staining (400×). G Number of apoptotic cells in AH mice determined by TUNEL staining (400×). H AKR1B10 expression in hepatocytes of liver tissues from AH mice by IF (400×). For panel C–H, ten mice in each treatment. *p < 0.05 compared to the control group. Data are shown as the mean ± standard deviation of three technical replicates. Data between two groups were compared by unpaired t-test.
Fig 4: RV treatment promotes anti-atherosclerotic activity in atherosclerosis model mice. (A-F) Effects of RV treatment on (A) HMG-CoA reductase activity, (B) LDH levels, (C) CPK activity, (D) serum ALT levels, (E) serum AST levels and (F) serum ALP levels compared with the control. *P<0.05 and **P<0.01. RV, resveratrol; LDH, lactate dehydrogenase; CPK, creatine phosphokinase; ALT, alanine transaminase; AST, aspartate transaminase; ALP, alkaline phosphatase.
Fig 5: HF-MSCs relieved liver pathological damage and improved liver function.(A, B) HE staining and Masson staining in the three groups (n = 6). (C–E) Comparison of liver serological indices ALT, AST, and ALB in the three groups (n = 6). Scale bar (A, B) 50 µm. All data are shown as the means ± SD (One-way ANOVA, n = 3). *P < 0.05, **P < 0.01, ***P < 0.001.
Supplier Page from Abcam for Mouse AST ELISA Kit (Aspartate Aminotransferase)