TABLE 2.
Effect of salsalate treatment on hepatic oxidative stress parameters in Wistar control and prediabetic HHTg rats.
| Wistar | Wistar + SAL | HHTg | HHTg + SAL | PS | PT | PI | |
|---|---|---|---|---|---|---|---|
| TBARS, nmol/mgprot | 1.32 ± 0.13 | 1.22 ± 0.12 | 1.64 ± 0.10$ | 1.20 ± 0.06## | n.s. | 0.05 | n.s. |
| Conjugated dienes, nmol/mgprot | 32.0 ± 2.4 | 28.6 ± 2.2 | 41.6 ± 2.4$$ | 28.8 ± 1.2### | 0.05 | 0.001 | 0.05 |
| GSH, μmol/mgprot | 68.61 ± 4.33 | 71.31 ± 4.94 | 62.89 ± 2.56 | 73.06 ± 2.96# | n.s. | 0.05 | n.s. |
| GSSG, μmol/mgprot | 1.11 ± 0.10 | 1.27 ± 0.10 | 1.74 ± 0.16$$ | 1.22 ± 0.10## | 0.05 | n.s. | 0.01 |
| GSH/GSSG | 62.86 ± 3.11 | 56.97 ± 2.65 | 37.49 ± 3.10$$$ | 63.20 ± 6.12### | 0.05 | 0.05 | 0.01 |
| SOD, U/mgprot | 0.16 ± 0.01 | 0.17 ± 0.01 | 0.11 ± 0.01$$ | 0.14 ± 0.01# | 0.01 | 0.05 | n.s. |
| GPx, μmol NADPH/min/mgprot | 276 ± 28 | 259 ± 20 | 222 ± 10 | 301 ± 27# | n.s. | n.s. | 0.05 |
| GR, nmol NADPH/min/mgprot | 166 ± 13 | 210 ± 29 | 133 ± 12 | 136 ± 13 | 0.01 | n.s. | n.s. |
Two-way ANOVA, results; PS, denotes the significance of Wistar vs. HHTg (strain effects), PT, denotes the significance of salsalate (treatment effects); PI, denotes the significance of salsalate in both strains (treatment vs. strain interaction). For multiple comparisons Fisher’s LSD, post hoc test was used; * denotes significance reflecting the effect of Wistar vs. Wistar + SAL, # denotes significance reflecting the effect of HHTg vs. HHTg + SAL, $ denotes significance reflecting the effect of Wistar vs. HHTg, n.s. denotes not significant; # p˂0.05, ## p˂0.01, ### p < 0.001; $ p˂0.05, $$ p˂0.01, $$$ p˂0.001. Data are mean ± SEM; n = 8 for each group. HHTg, hereditary hypertriglyceridemic rats; GSH, glutathione; GSSG, oxidized form of glutathione; SOD, superoxide dismutase; GPx, glutathioneperoxidase; GR, glutathione reductase; TBARS, thiobarbituric acid-reactive substance.