Fig 1: Dex protected hepatic I/R injury in vivo. The rat model of hepatic I/R was established. A, miR‐494 and JUND expression was detected using RT‐qPCR. B, The levels of ALT and AST in serum of rats were detected using ELISA. C, The rat liver sections were stained with HE staining. D, The rat liver sections were stained with immunohistochemical staining. E, The changes of JUND, p‐AKT, AKT, Nrf2 and NLRP3 were detected using Western blotting. N = 6. Data were presented as mean ± standard deviation and analysed using one‐way ANOVA, followed by Tukey's multiple comparison test, *** p < 0.001
Fig 2: (A,B) Liver/tibia ratio, (C,D) plasma levels of aspartate aminotransferase (AST), (E,F) plasma levels of alanine transaminase (ALT), and (G,H) ratio of AST/ALT from sedentary (SED) or exercise-preconditioned (EX) male (left) and female (right) rats treated with doxorubicin (DOX) or saline. Data are presented as mean ± SEM. Two-way ANOVA differences are indicated below the graphs. Circles indicate individual data points. * = significant difference between groups (p < 0.05). ** = significant difference between groups (p < 0.01), *** = significant difference between groups (p < 0.001).
Fig 3: Showing the effect of DOX and HES on all tested cardiac biomarkers; Troponin I (CTnI), CK-Total, CK-MB, LDH and AST for all experimental groups. According to Duncan multiple test, the different letters (a–c) are significantly different between treatments at the P < 0.05 level.
Fig 4: Inhibition of hepatic fibrosis by CTL under in vivo conditions. CCl4-induced rat hepatic fibrosis models were treated with different concentrations of CTL (0.5, 1.0 and 1.5 g/kg/day). (A) Hematoxylin and eosin staining and (B) Masson staining showing that CTL can ameliorate CCl4-induced liver histopathological injury. Red arrows represent extensive inflammatory cell infiltration, black arrows represent dense collagen fiber deposition and yellow arrows represent fibrous septa (magnification, ×200; scale bar, 50 µm). (C) AST and (D) ALT levels measured by ELISA. (E) Protein expression levels of E-cadherin, α-SMA, and SOX-9, as measured using western blot analysis. (F) Colla1 and (G) α-SMA mRNA levels as measured using reverse transcription-quantitative PCR. (H) Hydroxyproline level measured using ELISA. Results are presented as the mean ± SD (n=8), using one-way ANOVA. *P<0.05, **P<0.01 and ***P<0.001. ns, not significant; CTL, Carthamus tinctorius L.; HE, hematoxylin and eosin; AST, aspartate transaminase; ALT, alanine transaminase; α-SMA, α-smooth muscle actin; Colla1, collagen I, CTL-L, CTL low-dose group; CTL-M, CTL medium-dose group; CTL-H, CTL high-dose group.
Fig 5: Worm burden, antibodies, and liver damage assessment. Samples were harvested following two different treatment time points. Adult C. sinensis worms were recovered from the bile ducts of rats and quantified to calculate worm recovery (A). ELISA was performed using the sera (B) and duodenal samples (C) of rats to determine C. sinensis-specific antibody responses. ALT (D) and AST (E) concentrations in serum samples were evaluated. Statistical significances are indicated using asterisks (* p < 0.05, ** p < 0.01).
Supplier Page from Abcam for Rat AST ELISA Kit (Aspartate Aminotransferase)