NQO1 Antibody - #DF6437

Fig. 5. Effect of treatments of MGO, Que-mono-MGO, and Que-di-MGO on the expression levels of apoptotic markers and components of AKT and Nrf2-HO-1/NQO-1 signaling pathways. Significant differences (p < 0.05) between samples of different treatments are marked with different letters on each column.

Fig. 8. A. WB analysis was performed to observe Moschus’ effects on Keap1, NQO-1, Nrf-2, and OH-1 protein levels in the injured model. PC12 cells were processed with 70 μM H2O2 after pretreatment with a specific concentration of Moschus. (Model: 70 μM H2O2-treated PC12 cells, VC: 100 μM L-ascorbate-treated PC12 cells). (A) The ratio between Keap1 and β-actin (n = 3). (B) The ratio between NQO-1 and β-actin (n = 3). (C) The ratio between Nrf-2 and β-actin (n = 3). (D) The ratio between OH-1 and β-actin (n = 3). 1: Control 2: Model 3: Moschus-0.05 mg/ml 4: Moschus-0.1 mg/ml 5: Moschus-0.15 mg/ml 6: VC. Dates were represented as means ± SEM. * p < 0.05, * * p < 0.01, and * ** p < 0.001 vs the model group.

Fig. 2.| Pretreatment with monotropein protected against renal oxidative stress induced by cisplatin. The level of serum GSH(A). The level of serum MDA(B). The level of serum SOD(C). The level of serum CAT(D). The protein expressions of Nrf2, HO-1 and NQO1 (E) were detected by Western blot in kidney tissue.

FIGURE 7 |Effects of different doses of echinacoside (ECH) on the expressions of nuclear factor E2 p45‐related factor 2 (Nrf2), heme oxygenase‐1 (HO‐1), NAD(P)H:quinone oxidoreductase 1 (NQO1), and γ‐glutamyl cysteine synthetase (γ‐GCS) in the mice exposed to hypobaric hypoxia in protein level. Hippocampi of the mice were collected, and the protein levels of Nrf2 (cytoplasmic and nuclear), HO‐1, NQO1, and γ‐GCS were evaluated by Western blot. *p < 0.05, **p < 0.01 versus control; #p < 0.05, ##p < 0.01 versus hypoxia (HYP)

Figure 4. |Protein expression of genes related to antioxidant, adipogenic differentiation and beiging of the WAT in the retroperitoneal depot was detected by western-blot.(a) CHP upregulation protein expression of anti-oxidation-related genes in obese mice induced by HFD

Fig. 6.| Effect of PQQ on protein expression in the Nrf2/HO-1 pathway. The expression levels of Nrf2 (A), HO-1 (B), GCLM (C), and NQO1 (D). Data are shown as mean ± SD, n = 8. #p < 0.05 and ##p < 0.01 versus the Control group. ⁎p < 0.05 and ⁎⁎p < 0.01 versus the Model group.

Figure 7. Melatonin could attenuate the downregulation of MT1, MT2, and SIRT1/Nrf2 antioxidant signaling by cisplatin in mouse testes. (A) Melatonin level in mouse serum. (B) Melatonin level in mouse testes. (C) Determination of the ASMT and AANAT protein levels was performed by Western blotting in mouse testes. The blots were quantified using Image J software. (D) MT1 immunofluorescence in mouse testicular tissue. 3β-HSD was tagged with green fluorescence, while MT1 was tagged with red fluorescence. The nucleus was labeled with DAPI (scale bar = 20 μm). (E) MT2 immunofluorescence in mouse testicular tissue. 3β-HSD was tagged with red fluorescence, while MT2 was tagged with green fluorescence. The nucleus was labeled with DAPI (scale bar = 20 μm). (F) Determination of the MT1 and MT2 protein levels was performed by Western blotting in mouse testes. The blots were quantified using Image J software. (G) Determination of Nrf2, HO-1, and NQO1 protein levels was performed by Western blotting in mouse testes. The blots were quantified using Image J software. (H) Determination of SIRT1, SOD1, and SOD2 protein levels was performed by Western blotting in mouse testes. The blots were quantified using Image J software. CP, cisplatin. CP + Mel, cisplatin + melatonin. Mel, melatonin. Data are presented as the mean ± SEM (N = 8 per group). * p < 0.05 compared with controls or CP groups. ** p < 0.01 compared with controls or CP groups.