Journal: Food Science & Nutrition

Article Title: Nobiletin Ameliorates Skeletal Muscle Performance in D‐Galactose‐Induced Aging Mice by Boosting Aerobic Metabolism

doi: 10.1002/fsn3.71416

Figure Lengend Snippet: Nob improved the antioxidant capacity of skeletal muscle in D‐gal‐induced aging mice. (A) ROS content, n = 3 mice/group; (B) SOD activity, n = 4 mice/group; (C) MDA content, n = 4 mice/group; (E–G) Western blot analysis of SIRT1, PGC‐1α, Nrf2, and GAPDH in D‐gal‐induced C2C12 cells treated with vehicle and Nob, n = 3. ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: The PGC‐1α monoclonal antibody (66369‐1‐Ig), NRF2 Rabbit mAb (16396‐1‐AP), SIRT1 polyclonal antibody (13161‐1‐AP), MFN1 Polyclonal antibody (13798‐1‐AP), OPA1 Polyclonal antibody (27733‐1‐AP), and Beta Tubulin Polyclonal antibody (10094‐1‐AP) were purchased from Proteintech (Wuhan, China).

Techniques: Activity Assay, Western Blot

Journal: Frontiers in Immunology

Article Title: Cigarette smoke exposure triggers dendritic cell-derived exosome-mediated Th17 and Treg polarization through an autophagy- and necroptosis-associated SIRT1-dependent mechanism in vitro

doi: 10.3389/fimmu.2025.1715736

Figure Lengend Snippet: The expression of SIRT1 in dendritic cells (DCs) was significantly reduced following cigarette smoke treatment when compared with the respective control groups at various time points. Specifically, SIRT1 expression in the CSE-treated DC group was reduced at 12 h, 24 h, 36 h, and 48 h compared to that in the untreated DC group at the corresponding time points (**Comparison with the DC 4 h group, p< 0.01; ***Comparison with the DC 4 h group, p < 0.001; ****Comparison with the DC 4 h group, p < 0.0001; ###Comparison with the DC 12 h group, p < 0.001; $$$$Comparison with the DC 24 h group, p < 0.0001; §§§§Comparison with the DC 36 h group, p < 0.0001; &&&&Comparison with the DC 48 h group, p < 0.0001). For western blot analyses, values are given as mean ± SD of at least three independent experiments (n = 3), and the results were analyzed using unpaired two-tailed Student’s t-tests.

Article Snippet: The SIRT1 activator SRT1720 was purchased from MedChemexpress (MedChemexpress Biotechnology Company, USA).

Techniques: Expressing, Control, Comparison, Western Blot, Two Tailed Test

Journal: Frontiers in Immunology

Article Title: Cigarette smoke exposure triggers dendritic cell-derived exosome-mediated Th17 and Treg polarization through an autophagy- and necroptosis-associated SIRT1-dependent mechanism in vitro

doi: 10.3389/fimmu.2025.1715736

Figure Lengend Snippet: Data from western blot experiments are given as the mean ± SD of at least three independent experiments (n = 3) for panels (a–h) . Compared with the DC group, **** p < 0.0001. Compared with the SRT1720 + DC group, #### p < 0.0001. Compared with the CSE + DC group, && p < 0.01, &&& p < 0.001, &&&& p < 0.0001. Statistical comparisons were performed using ANOVA followed by the Newman−Keuls post hoc test for multiple comparisons.

Article Snippet: The SIRT1 activator SRT1720 was purchased from MedChemexpress (MedChemexpress Biotechnology Company, USA).

Techniques: Western Blot

Journal: Molecular Medicine Reports

Article Title: High-intensity exercise training inhibits excessive autophagy in the hyperlipidemic myocardium of ApoE -/- mice via the NAD + -mediated SIRT1/MFN2 pathway

doi: 10.3892/mmr.2025.13753

Figure Lengend Snippet: NAD + ameliorates cardiac damage in hyperlipidemic mice by modulating the SIRT1/MFN2 pathway. (A) Protein interaction analysis. (B) Expression levels of SIRT1 and MFN2 proteins in the heart tissues of mice. (C) Representative immunohistochemistry images showing the expression of SIRT1 and MFN2 in myocardial tissue. The arrows indicate areas of stained cells. Scale bar, 100 µm; magnification, ×40. (D) SIRT1 and MFN 2 were detected by immunofluorescence double staining to assess colocalization. Scale bars, 100 and 50 µm; magnification, ×40. Data are presented as the mean ± standard error of the mean (n=3); statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. *P<0.05, **P<0.01, ***P<0.001. HFD, high-fat diet; MFN2, mitofusin 2; NAD + , nicotinamide adenine dinucleotide; ND, normal diet; SIRT1, sirtuin 1.

Article Snippet: To inhibit SIRT1 activity, cells were treated with 10 μM EX-527 (cat. no. HY-15452; MedChemExpress) for 24 h (37°C, 5% CO 2 ).

Techniques: Expressing, Immunohistochemistry, Staining, Immunofluorescence, Double Staining

Journal: Molecular Medicine Reports

Article Title: High-intensity exercise training inhibits excessive autophagy in the hyperlipidemic myocardium of ApoE -/- mice via the NAD + -mediated SIRT1/MFN2 pathway

doi: 10.3892/mmr.2025.13753

Figure Lengend Snippet: NAD + supplementation activates the PI3K/AKT/mTOR pathway in the myocardium. (A) TUNEL staining was performed to assess myocardial cell apoptosis in the heart tissues of mice. Magnification, ×40; scale bar, 100 µm. (B) Protein interaction analysis. Expression levels of (C) p-PI3K/PI3K, (D) p-AKT/AKT and (E) p-mTOR/mTOR in the heart tissues of mice. Data are presented as the mean ± standard error of the mean (n=4); statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. *P<0.05, **P<0.01. HFD, high-fat diet; Mfn2, mitofusin 2; NAD + , nicotinamide adenine dinucleotide; ND, normal diet; p-, phosphorylated; Sirt1, sirtuin 1.

Article Snippet: To inhibit SIRT1 activity, cells were treated with 10 μM EX-527 (cat. no. HY-15452; MedChemExpress) for 24 h (37°C, 5% CO 2 ).

Techniques: TUNEL Assay, Staining, Expressing

Journal: Molecular Medicine Reports

Article Title: High-intensity exercise training inhibits excessive autophagy in the hyperlipidemic myocardium of ApoE -/- mice via the NAD + -mediated SIRT1/MFN2 pathway

doi: 10.3892/mmr.2025.13753

Figure Lengend Snippet: NAD + protects ApoE −/− HL-1 cells from lipid accumulation and oxidative stress. (A) Cell viability was significantly enhanced in the 5 mM NAD + group compared with that in the control group. (B) NAD + supplementation reduced TC levels in ApoE −/− -treated cells. (C) TG levels were also significantly decreased by NAD + treatment. (D) LDL-C levels were also reduced in the ApoE −/− + NAD + group, indicating improved lipid metabolism. (E) NAD + supplementation increased GSH levels, reflecting enhanced antioxidant defense. (F) SOD activity was also significantly elevated in the ApoE −/− + NAD + group, suggesting improved oxidative stress response. (G) ROS staining revealed reduced reactive oxygen species in the ApoE −/− + NAD + group, indicating a decrease in oxidative stress. Scale bar, 200 µm. (H) Microscopic images confirmed improved cell morphology and viability in the ApoE −/− + NAD + group. Scale bar, 100 µm. (I) JC-1 staining showed improved mitochondrial membrane potential in the ApoE −/− + NAD + group. Scale bar, 100 µm. (J) Immunofluorescence staining demonstrated increased expression of SIRT1 in the ApoE −/− + NAD + group, suggesting activation of the SIRT1 pathway. Magnification, ×40; scale bar, 50 µm. Data are presented as the mean ± standard error of the mean (n=3); statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. *P<0.05, **P<0.01, ***P<0.001. ApoE −/− , apolipoprotein E-deficient; GSH, glutathione; LDL-C, low-density lipoprotein cholesterol; NAD + , nicotinamide adenine dinucleotide; ROS, reactive oxygen species; SIRT1, sirtuin 1; SOD, superoxide dismutase; TC, total cholesterol; TG, triglycerides.

Article Snippet: To inhibit SIRT1 activity, cells were treated with 10 μM EX-527 (cat. no. HY-15452; MedChemExpress) for 24 h (37°C, 5% CO 2 ).

Techniques: Control, Activity Assay, Staining, Membrane, Immunofluorescence, Expressing, Activation Assay

Journal: Molecular Medicine Reports

Article Title: High-intensity exercise training inhibits excessive autophagy in the hyperlipidemic myocardium of ApoE -/- mice via the NAD + -mediated SIRT1/MFN2 pathway

doi: 10.3892/mmr.2025.13753

Figure Lengend Snippet: NAD + enhances MFN2/SIRT1 expression and activates the PI3K/AKT pathway in HL-1 cells. (A) Representative immunofluorescence double staining showing colocalization of MFN2 and SIRT1 in HL-1 cells. Magnification, ×40; scale bars, 100 and 50 µm. Protein expression levels of (B) SIRT1 and MFN2, (C) PI3K and p-PI3K, (D) AKT and p-AKT, and (E) mTOR and p-mTOR in HL-1 cells. Data are presented as the mean ± SEM (n=4); statistical analysis was performed using one-way ANOVA followed by Tukey's post hoc test. *P<0.05, **P<0.01, ***P<0.001. ApoE −/− , apolipoprotein E-deficient; MFN2, mitofusin 2; NAD + , nicotinamide adenine dinucleotide; p-, phosphorylated; SIRT1, sirtuin 1.

Article Snippet: To inhibit SIRT1 activity, cells were treated with 10 μM EX-527 (cat. no. HY-15452; MedChemExpress) for 24 h (37°C, 5% CO 2 ).

Techniques: Expressing, Immunofluorescence, Double Staining

Journal: Molecular Medicine Reports

Article Title: High-intensity exercise training inhibits excessive autophagy in the hyperlipidemic myocardium of ApoE -/- mice via the NAD + -mediated SIRT1/MFN2 pathway

doi: 10.3892/mmr.2025.13753

Figure Lengend Snippet: Mechanistic overview of NAD + in improving HFD-induced cardiac dysfunction. High-intensity interval training elevates cardiac NAD + levels, and subsequent intraperitoneal NAD + supplementation further activates SIRT1/MFN2 signaling. This enhances PI3K/AKT/mTOR phosphorylation, promoting autophagy and mitochondrial quality control. Interventions also improve lipid metabolism, reducing TG, T-CHO, and LDL-C. Together, these mechanisms mitigate mitochondrial dysfunction, and metabolic disturbances in HFD-induced cardiac injury. LDL-C, low-density lipoprotein cholesterol; MFN2, mitofusin 2; NAD + , nicotinamide adenine dinucleotide; T-CHO, total cholesterol; TG, triglycerides; SIRT1, sirtuin 1.

Article Snippet: To inhibit SIRT1 activity, cells were treated with 10 μM EX-527 (cat. no. HY-15452; MedChemExpress) for 24 h (37°C, 5% CO 2 ).

Techniques: Phospho-proteomics, Control