NRF1 Antibody - #AF5298

Fig. 5 Adipose tissue-specific omentin overexpression inhibited WNT5A/Ca2+ signaling pathway and improved mitochondrial biogenesis to ameliorate myocardial injury in HF mice. (A) Serum omentin level of HF patients and healthy subjects. A total of 58 HF patients and 38 healthy subjects were enrolled. (B) The omentin serum content of adipose tissue-specific omentin overexpression by intravenous injection of AAV-omentin and negative control by intravenous injection of AAV-NC (n = 8). (C) The expression of omentin in the inguinal fat of mice with adipose tissue-specific omentin overexpression was detected by immunohistochemistry (n = 4). Scale bar = 200 μm. (D) Representative echocardiographs of mice with AAV-omentin overexpression and the statistical results of (E) LV EF, (F) LV FS, (G) stroke volume, (H) LVPW; d, (I) IVS; d, (J) RWT and (K) LV Mass were presented (n = 8). (L) Representative TTC staining images of heart tissues of mice with AAV-omentin overexpression (n = 6). (M) Representative images of H&E and Masson staining of heart tissues of mice with AAV-omentin overexpression (n = 3), scale bar = 250 μm. (N) The serum content of BNP in mice with AAV-omentin overexpression (n = 8). (O) The serum CK activity in mice with AVV-omentin overexpression (n = 8). (P) The protein expression level of WNT5A, Frizzled2 and p-CAMKII/CAMKII were determined by Western blot. β-actin was used as a loading control (n = 5). (Q) The protein expression level of PGC-1α, NRF1, NRF2 and TFAM were determined by Western blot in mice with AAV-omentin overexpression. β-actin was used as a loading control (n = 5). Values are expressed as the means ± SD. (A) Unpaired Student's two-tailed t-test; (B–Q) One-way ANOVA followed by the Dunnett's post hoc test. #P < 0.05, ##P < 0.01, ###P < 0.001 vs. Sham; *P < 0.05, **P < 0.01, ***P < 0.001 vs. CAL.

Fig. 6. Hsp22 regulates PGC1α via AMPK signaling pathway in rats after SAH Beam balance scores, Modified Garcia scores and Brainwater content in various groups. n = 6 per group. (B) Representative photomicrographs of TUNEL staining and quantitative analyses in the indicated groups. n = 4 per group. Scale bar = 100 μm. (C) Typical photomicrographs showing double immunofluorescence staining of PGC1α (green) and NeuN (red) in diverse experimental groups. n = 4 per group. Scale bar = 50 μm. (D) Western blot images and quantitative analyses of p-AMPK/AMPK, PGC1α, Drp1, Nrf1, TFAM, UCP2, Cleaved caspase-3/Caspase-3, Bcl2, Bax, Cytosolic and mitochondrial cytochrome c. n = 6 per group. Bars represent mean ± SD. **P < 0.01, *P < 0.05 vs. Sham group. ##P < 0.01, #P < 0.05 vs. SAH + Vehicle group. &&P < 0.01, &P < 0.05 vs. SAH + hsp22+scramble siRNA. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)

Figure 6. Changes in mitochondrial-related indexes after PARK7 silencing. (A) Changes in mitochondrial synthesis proteins in APAP-treated L02 cells with and without PARK7 silencing and statistical analysis, N = 3. * p < 0.05 vs. ShNC group, ** p < 0.01 vs. ShNC group, # p < 0.05vs. ShNC+APAP group, ## p < 0.01 vs. ShNC+APAP group. (B) WB and statistical analysis of the mitochondrial synthetic proteins PGC-1α, NRF1 and TFAM in the liver tissue of mice with or without APAP intervention with PARK7 knockdown, N = 3, * p < 0.05 vs. WT group, ** p < 0.01 vs. WT group, ## p < 0.01 vs. WT+APAP group. (C,D) Changes in mitochondrial respiratory function and glycolytic function under APAP intervention with or without PARK7 silencing, N = 3. * p < 0.05 vs. shNC group, ** p < 0.01 vs. shNC group, # p < 0.05 vs. shNC+APAP group, ## p < 0.01 vs. shNC+APAP group.

Fig. 5. |Mitochondrial function were downregulated in ApoE−/−-HFD mice. (A–D)Representative immunoblots and relative protein levels of PGC1α and NRF1. (E–F)Hepatic expression and relative flourescent intensity of ROS by immunofluorescent staining.

Fig. 6 Characterization of lipid and glucose metabolism in intermuscular adipose tissues (IMATs). Representative western blots (A, C, E, G, I) and quantification of the gene-expression levels of peroxisome proliferators-activated receptor-γ (PPAR-γ) (B), phosphorylated PPAR-γ (p-PPAR-γ; Ser112) (F), nuclear respiratory factor-1 (NRF-1) (J), glucose transporter-4 (GLUT-4) (D), glucose transporter-1 (GLUT-1) (H), and perilipin-5 (Plin-5) (K). The data represent the mean ± the standard error of the mean (n = 5–6/group). CON control, EMA combined therapies + compound-c, EMC combined therapies, EXE moderate exercise, GAPDH glyceraldehyde-3-phosphate dehydrogenase, MET metformin, PRE prediabetes. ap