Journal: Journal of Sport and Health Science

Article Title: Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice

doi: 10.1016/j.jshs.2025.101100

Figure Lengend Snippet: Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

Article Snippet: Primary antibodies used for analysis were from Cell Signaling Technologies (Danvers, MA, USA) and diluted 1:1000 unless otherwise stated as follows: protein kinase B (Akt; 1:500; #4691; Cell Signaling Technologies), phospho-Akt (pAkt) S473 (1:500; #9271; Cell Signaling Technologies), Ubiquitin (#3933; Cell Signaling Technologies), microtubule-associated protein light chain 3 (LC3 II/I; #4018; Cell Signaling Technologies), cytochrome c oxidase subunit 4(COX4; #11967; Cell Signaling Technologies), Akt substrate 160 (AS160 S318; #8619; Cell Signaling Technologies), AS160 T642 (#8881; Cell Signaling Technologies), eukaryotic translation initiation factor 4E binding protein (4E-BP1; #9452; Cell Signaling Technologies), and glyceraldehyde 3 phosphate dehydrogenase (GAPDH; #2118; Cell Signaling Technologies).

Techniques: Phospho-proteomics, Injection, Western Blot, Muscles, Ubiquitin Proteomics, Staining, Binding Assay

Journal: Journal of Sport and Health Science

Article Title: Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice

doi: 10.1016/j.jshs.2025.101100

Figure Lengend Snippet: Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

Article Snippet: Primary antibodies used for analysis were from Cell Signaling Technologies (Danvers, MA, USA) and diluted 1:1000 unless otherwise stated as follows: protein kinase B (Akt; 1:500; #4691; Cell Signaling Technologies), phospho-Akt (pAkt) S473 (1:500; #9271; Cell Signaling Technologies), Ubiquitin (#3933; Cell Signaling Technologies), microtubule-associated protein light chain 3 (LC3 II/I; #4018; Cell Signaling Technologies), cytochrome c oxidase subunit 4(COX4; #11967; Cell Signaling Technologies), Akt substrate 160 (AS160 S318; #8619; Cell Signaling Technologies), AS160 T642 (#8881; Cell Signaling Technologies), eukaryotic translation initiation factor 4E binding protein (4E-BP1; #9452; Cell Signaling Technologies), and glyceraldehyde 3 phosphate dehydrogenase (GAPDH; #2118; Cell Signaling Technologies).

Techniques: Phospho-proteomics, Injection, Western Blot, Muscles, Ubiquitin Proteomics, Staining, Binding Assay

Journal: Journal of Sport and Health Science

Article Title: Weightlifting outperforms voluntary wheel running for improving adiposity and insulin sensitivity in obese mice

doi: 10.1016/j.jshs.2025.101100

Figure Lengend Snippet: Resistance exercise exceeds the benefits of endurance exercise in ameliorating metabolic dysfunction. Following 8 weeks of diet and exercise interventions, all mice were assessed for their metabolic function by GTT, ITT, and skeletal muscle response of Akt and AS160 phosphorylation to injection of insulin measured by Western blot. (A–C) HOMA-IR taken after an overnight fast for baseline glucose and insulin. (D and E) GTT from 0–120 min and calculated AUC; colored * indicates significant difference from NC-SED. (F and G) ITT from 0–60 min and calculated AUC; colored * indicates significant difference from NC-SED. (H–N) pAkt stimulation, AS160 S318, and AS160 T642 in hindlimb muscles before and after insulin injection and the pre–post ∆ in phosphorylation. (O and P) Total and phosphorylated 4E-BP1. (Q–T) Western results for Raptor, COX4, LC3 II/I, and ubiquitin staining. Representative western blot images inset right. Data presented as mean ± standard error of the mean. Statistical analysis performed by analysis of variance between groups: * p < 0.05, ** p < 0.01, *** p < 0.001, and **** p < 0.0001. NC-SED n : 8–16 (white); HFD-SED n : 8–18 (red); HFD-R EX n : 8–16 (blue); HFD-E EX n : 8–15 (green). 4E-BP1 = Eukaryotic translation initiation factor 4E binding protein; Akt = protein kinase B; AS160 = Akt substrate 160; COX4 = cytochrome c oxidase 4; CS = citrate sythase; E EX = endurance exercise; GAPDH = glyceraldehyde 3 phosphate dehydrogenase; GTT = glucose tolerance test; HFD = high fat diet; HOMA-IR = homeostatic model assessment for insulin resistance; iAUC = integrated area under the curve; ITT = insulin tolerance test; LC3 II/I = microtubule-associated protein light chain 3; NC = normal chow; pAkt = phospho-Akt; R EX = resistance exercise; SED = sedentary; Ub = ubiquitin.

Article Snippet: Primary antibodies used for analysis were from Cell Signaling Technologies (Danvers, MA, USA) and diluted 1:1000 unless otherwise stated as follows: protein kinase B (Akt; 1:500; #4691; Cell Signaling Technologies), phospho-Akt (pAkt) S473 (1:500; #9271; Cell Signaling Technologies), Ubiquitin (#3933; Cell Signaling Technologies), microtubule-associated protein light chain 3 (LC3 II/I; #4018; Cell Signaling Technologies), cytochrome c oxidase subunit 4(COX4; #11967; Cell Signaling Technologies), Akt substrate 160 (AS160 S318; #8619; Cell Signaling Technologies), AS160 T642 (#8881; Cell Signaling Technologies), eukaryotic translation initiation factor 4E binding protein (4E-BP1; #9452; Cell Signaling Technologies), and glyceraldehyde 3 phosphate dehydrogenase (GAPDH; #2118; Cell Signaling Technologies).

Techniques: Phospho-proteomics, Injection, Western Blot, Muscles, Ubiquitin Proteomics, Staining, Binding Assay

Journal: Materials Today Bio

Article Title: Intrinsic AIE drug nanocrystals enable imaging-guided orchitis theranostics

doi: 10.1016/j.mtbio.2026.103639

Figure Lengend Snippet: In vitro anti-inflammatory evaluation of the nanocrystals in lipopolysaccharide (LPS)-stimulated cells. (A–C) CCK-8 assay showing the effects of PNPs, ZNPs, and MNPs on cell viability. (D–F) ELISA quantification of the pro-inflammatory cytokines TNF-α, IL-1β, and IL-6 in culture supernatants. (G–I) Western blot analysis of phosphorylated p65 (p-p65) and inhibitor of κBα (IκBα) expression and corresponding densitometric quantification. (J) Immunofluorescence detection of p65 nuclear translocation. (K) DCFH-DA probe measurement of intracellular reactive oxygen species (ROS) generation. Data: mean ± SEM; ** p < 0.01, *** p < 0.001.

Article Snippet: Antibodies against NF-κB p65 (Proteintech, 10745-1-AP), MyD88 (Proteintech, 67969-1-Ig), phospho-NF-κB p65 (Abclonal, AP1294), TLR4 (Proteintech, 19811-1-AP), IκBα (Abclonal, A19714), GAPDH (Abclonal, A19056), PK2 and PKR1 were used for immunofluorescence, immunohistochemistry or western blotting as appropriate.

Techniques: In Vitro, CCK-8 Assay, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Immunofluorescence, Translocation Assay

Journal: Materials Today Bio

Article Title: Human iPSC-EV-loaded nanofiber stent coatings accelerate vascular repair by enhancing EGFR/HIF-1α signaling and suppressing ROCK1-mediated remodeling

doi: 10.1016/j.mtbio.2026.103564

Figure Lengend Snippet: In vivo evaluation of re-endothelialization and inhibition of intimal hyperplasia following stent implantation. (A–E) SEM images of the luminal surface treated with EV-loaded (A, B) or DPBS-loaded (D, E) nanofibrous membranes. The EV-treated group exhibited a continuous, smooth, and intact endothelial layer (A, B), whereas the DPBS group displayed incomplete coverage with substantial endothelial disruption (D, E). (C, F) H&E-stained cross-sections revealed the extent of neointimal formation above the stent struts (black arrows). The EV group (C) demonstrated significantly reduced intimal thickening compared with the pronounced hyperplasia observed in the DPBS group (F). (G–H) Statistical analysis confirmed that EV treatment significantly increased endothelial coverage (G) and suppressed intimal hyperplasia thickness (H). (I–K) EV treatment significantly upregulated the expression of the angiogenic factor VEGF (I), the endothelial marker CD31 (J), and the proliferation marker PCNA (K), confirming accelerated vascular repair. (L–N) EV treatment prevented phenotypic switching and matrix accumulation, as evidenced by reduced levels of the contractile/hyperplasia marker α-SMA (L). Furthermore, the EV group showed decreased expression of matrix metalloproteinases MMP-2 and MMP-9 (M) and beneficial modulation of collagen composition, with increased Collagen I and the Collagen I/III ratio (N). (O–P) The EV group exhibited significantly downregulated levels of the profibrotic factor TGF-β1 (O) and the inflammatory cytokine IL-6 (P). N = 5 (G and H), and n = 3 (I-P). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.000.

Article Snippet: Smooth muscle and fibrosis markers: α-SMA (1:1000, A17910, ABclonal), SM22α (1:1000, ab14106, Abcam), Calponin-1 (1:1000, ab46794, Abcam), Osteopontin (1:1000, ab8448, Abcam), Collagen I (1:1000, A5786, ABclonal), and Collagen III (1:1000, A3795, ABclonal).

Techniques: In Vivo, Inhibition, Disruption, Staining, Expressing, Marker

Journal: International Dental Journal

Article Title: Hypoxia-Inducible Factor-1α Stabilization Alleviates Hypoxia-Induced Temporomandibular Joint Osteoarthritis by Activating MDM2 to Suppression of p53 Signalling

doi: 10.1016/j.identj.2026.109805

Figure Lengend Snippet: DMOG-mediated HIF-1α stabilization exerts a protective effect by inhibiting p53 signalling transduction. (A) Volcano plot of DEGs in chondrocytes treated with or without DMOG ( P < .05, |fold change| > 2) under hypoxic conditions. (B) KEGG pathway enrichment analysis of DEGs. (C) Representative immunohistochemical images of p53 in condylar chondrocytes (scale bar: 100 μm) and quantitative analysis of p53-positive area ( n = 6). (D and E) Western blot and quantitative analysis of HIF-1α, p53, p21, and BAX protein levels in chondrocytes under hypoxia and hypoxia + DMOG conditions. (F and G) Western blot images and quantitative analysis of iNOS, HIF-1α, MMP13, p53, p21, BAX, and TNF-α protein levels in chondrocytes under hypoxia, hypoxia + DMOG, and hypoxia + DMOG + NSC-207895 (HX + DMOG + NSC-207895) conditions ( n = 3). (H) Immunofluorescence staining images and quantitative analysis of IL-6 and MMP3 in chondrocytes treated with DMOG and NSC-207895 under hypoxia ( n = 3). Scale bar: 50 μm. Data are presented as mean ± SEM. Statistical significance was determined by unpaired Student’s t test (for pairwise comparisons) or one-way ANOVA (for multigroup comparisons), as appropriate. ns, no significance, * P < .05, ** P < .01, *** P < .001, **** P < .0001.

Article Snippet: The membranes were blocked with 5% nonfat milk and incubated with the following primary antibodies: HIF-1α (1:1000; Abcam), p53 (1:1000; ABclonal), TNF-α (1:1000; Huabio), MMP13 (1:1000; Abcam), iNOS (1:1000; Servicebio), BAX (1:1000; Proteintech), p21 (1:1000; Abcam), MDM2 (1:1000; Immunoway), and α-Tubulin (1:5000; Servicebio).

Techniques: Transduction, Immunohistochemical staining, Western Blot, Immunofluorescence, Staining

Journal: International Dental Journal

Article Title: Hypoxia-Inducible Factor-1α Stabilization Alleviates Hypoxia-Induced Temporomandibular Joint Osteoarthritis by Activating MDM2 to Suppression of p53 Signalling

doi: 10.1016/j.identj.2026.109805

Figure Lengend Snippet: Stabilized HIF-1α transcriptionally activates Mdm2 to promote p53 ubiquitin-proteasomal degradation in hypoxic condylar. (A) Co-IP assay detecting endogenous p53 ubiquitination in hypoxic chondrocytes treated with or without 1 mM DMOG. (B and C) qRT-PCR analysis of Tp53 and Mdm2 mRNA expression in chondrocytes cultured under hypoxia with or without DMOG intervention. (D) Reciprocal Co-IP assay for detecting physical interaction between MDM2 and p53 in hypoxic chondrocytes with or without DMOG treatment. (E) Western blot analysis of p53 protein abundance in hypoxic chondrocytes incubated with DMOG in the presence or absence of 10 μM MG132. (F) JASPAR database-based in silico prediction of potential HIF-1α binding sites on rat Mdm2 promoter. (G) ChIP-qPCR assay measuring HIF-1α occupancy on the Mdm2 promoter in hypoxic chondrocytes with or without DMOG. (H) Schematic diagram. Data are presented as mean ± SEM ( n = 3 per group). Statistical significance was determined by unpaired Student’s t test. ** P < .01, *** P < .001.

Article Snippet: The membranes were blocked with 5% nonfat milk and incubated with the following primary antibodies: HIF-1α (1:1000; Abcam), p53 (1:1000; ABclonal), TNF-α (1:1000; Huabio), MMP13 (1:1000; Abcam), iNOS (1:1000; Servicebio), BAX (1:1000; Proteintech), p21 (1:1000; Abcam), MDM2 (1:1000; Immunoway), and α-Tubulin (1:5000; Servicebio).

Techniques: Ubiquitin Proteomics, Co-Immunoprecipitation Assay, Quantitative RT-PCR, Expressing, Cell Culture, Western Blot, Quantitative Proteomics, Incubation, In Silico, Binding Assay, ChIP-qPCR