Journal: Frontiers in Nutrition

Article Title: Astaxanthin alleviates altered hepatic lipid metabolism and oxidative stress in animals fed a high-sucrose diet

doi: 10.3389/fnut.2026.1781406

Figure Lengend Snippet: (A) Representative photomicrographs of p-NFκB p65 immunocytochemical staining in liver tissues (400 × magnification), and (B) quantitative immunohistochemical analysis of p-NFκB p65 expression in the liver of rats fed a reference diet (RD), RD plus ASTX (RD + ASTX), high-sucrose diet (HSD), and HSD plus ASTX (HSD + ASTX). Values (mean ± SEM, n = 6 ) are expressed as the in tegrated optical density (IOD). Values that do not share the same letter were significantly different ( p < 0.05) when one variable at a time was compared by two-way ANOVA. D, effect of Diet. I, effect of intervention. Int (D x I), interaction between diet x intervention. ns, not significant.

Article Snippet: The samples were incubated in a humid chamber first with a specific primary antibody for Nrf2 (mouse monoclonal antibody; sc-365949; Santa Cruz Biotechnology) and p-NFκB p65 (mouse monoclonal antibody; sc-136548; Santa Cruz Biotechnology) (for 14–16 h at 4 °C) and then with biotin-conjugated secondary antibody (antimouse, 1:100 dilution, Sigma) for 30 min at room temperature.

Techniques: Staining, Immunohistochemical staining, Expressing

Journal: Frontiers in Nutrition

Article Title: Astaxanthin alleviates altered hepatic lipid metabolism and oxidative stress in animals fed a high-sucrose diet

doi: 10.3389/fnut.2026.1781406

Figure Lengend Snippet: Mechanisms by which ASTX modulates liver lipid metabolism and oxidative stress in HSD-fed rats. ASTX supplementation mitigates hepatic injury by reducing steatosis and triglyceride accumulation, mainly through enhanced mitochondrial fatty acid β-oxidation (↑ CPT-1 activity) without affecting lipogenesis. In parallel, ASTX improves hepatic redox homeostasis by lowering ROS levels, increasing antioxidant enzyme activities (CAT, GST) and restoring GSH content. Increased Nrf2 and decreased p-NFκB p65 protein expression were also modulated by ASTX treatment. Solid lines indicate effects supported by the experimental data, whereas dashed lines represent suggested pathways not directly evaluated in this study.

Article Snippet: The samples were incubated in a humid chamber first with a specific primary antibody for Nrf2 (mouse monoclonal antibody; sc-365949; Santa Cruz Biotechnology) and p-NFκB p65 (mouse monoclonal antibody; sc-136548; Santa Cruz Biotechnology) (for 14–16 h at 4 °C) and then with biotin-conjugated secondary antibody (antimouse, 1:100 dilution, Sigma) for 30 min at room temperature.

Techniques: Activity Assay, Expressing

Journal: Cell cycle (Georgetown, Tex.)

Article Title: Sustained activation of NF-κB through constitutively active IKKβ leads to senescence bypass in murine dermal fibroblasts.

doi: 10.1080/15384101.2024.2325802

Figure Lengend Snippet: Figure 2. Expression of constitutively active IKKβ bypasses cellular senescence. (a) Control (R26StopFLIKK2CA Cre-negative) and IKKβ-CA (R26StopFLIKK2CA Sm22αCre) skin fibroblasts were treated with MG132 (10 μM), a proteasome inhibitor, for 30 min prior to stimulation with IL-1β (10 ng/ml) for 5 min. Whole-cell lysates were analyzed by Western blotting using the indicated antibodies. Representative images are shown (n = 3). (b) Nuclear and cytoplasmic fractions were prepared from control and IKKβ-CA skin fibroblasts and analyzed by Western blotting. Nuclear p65 levels were quantified by ImageJ and normalized to the level of Lamin A (n = 3). (c)(d) Growth curves of control and IKKβ-CA skin fibroblasts under 20% and 3% oxygen conditions (n = 5). P2 Skin fibroblasts isolated from five adult control and IKKβ-CA mice were passaged in parallel under 20% oxygen conditions according to a 3T3 protocol and under 3% oxygen conditions according to a 3T1 protocol. The graph shows the cumulative number of cells in sequential passages. (e)(f) Representative images and quantification of senescence-associated β- galactosidase (SA-β-gal) staining of control and IKKβ-CA cells in passage 8 cultured under 3% and 20% oxygen conditions (n = 5). Scale bars, 100 µm. Error bars represent the standard error of the mean. (*p value < 0.05, **p value < 0.01)

Article Snippet: Phospho-p53 (Ser20) (# PA5–104741), phospho-p53 (Ser37) (#HYP80843) and phospho-RelA/p65 (Ser276) (#NB100–82086) antibodies were purchased from Invitrogen, MedChemExpress and Novus Biologicals, respectively.

Techniques: Expressing, Control, Western Blot, Isolation, Staining, Cell Culture

Journal: Cell cycle (Georgetown, Tex.)

Article Title: Sustained activation of NF-κB through constitutively active IKKβ leads to senescence bypass in murine dermal fibroblasts.

doi: 10.1080/15384101.2024.2325802

Figure Lengend Snippet: Figure 3. Expression of nondegradable IκBα abolishes IKKβ-CA-induced senescence bypass. (a) Control (R26StopFLIKK2CA Cre-negative) and IKKβ-CA (R26StopFLIKK2CA Sm22αCre) skin fibroblasts were infected with lentivirus carrying an empty vector (EV) or FLAG-tagged IκBαSR. The expression of IκBαSR was confirmed by Western blotting using an antibody against the DYKDDDDK Tag. Representative images are shown (n = 4). (b) Nuclear and cytoplasmic fractions were prepared from control and IKKβ-CA skin fibroblasts harboring EV or IκBαSR. The nuclear p65 and p50 levels were measured by Western blotting, with quantification performed with ImageJ and normalized to the level of Lamin A (n = 4). (c)(d) Growth curves of control and IKKβ-CA skin fibroblasts harboring EV and IκBαSR cultured under 20% and 3% oxygen conditions, respectively. Skin fibroblasts were cultured under physiological oxygen level (3-5% oxygen) conditions until passage 3, at which time, they were infected with lentivirus. The cells were passaged again and treated with 2 μg/ml puromycin for 3 days under 3% oxygen conditions. The selected cells were passaged under 20% oxygen conditions according to a 3T2 protocol (c) or maintained under physiological oxygen level (3% oxygen) conditions according to a 3T1 protocol (d). The graph shows the cumulative number of cells in sequential passages. (e) Representative images and quantification of senescence-associated β-galactosidase (SA-β-gal) staining of control and IKKβ-CA cells harboring EV or IκBaSR cultured under 20% oxygen conditions. Scale bars, 100 µm. Error bars represent the standard error of the mean. (*p value < 0.05, **p value < 0.01)

Article Snippet: Phospho-p53 (Ser20) (# PA5–104741), phospho-p53 (Ser37) (#HYP80843) and phospho-RelA/p65 (Ser276) (#NB100–82086) antibodies were purchased from Invitrogen, MedChemExpress and Novus Biologicals, respectively.

Techniques: Expressing, Control, Infection, Plasmid Preparation, Western Blot, Cell Culture, Staining

Journal: Signal Transduction and Targeted Therapy

Article Title: Bioengineered iPSC-derived human macrophages with increased angiotensin-converting enzyme (ACE) expression suppress solid tumor growth

doi: 10.1038/s41392-026-02650-3

Figure Lengend Snippet: Determination of M1 vs. M2 polarization in iMac. a Pro-inflammatory M1 cytokines IL-1β, TNFα, IL-6, and IL-8 measured by ELISA. b Anti-inflammatory M2 cytokines IL-4, IL-10, IL-13, CCL5, CCL17, and CCL20 measured by ELISA. For a , b iMac were cultured in 6-well plates (3 × 10 6 cells/well). To challenge with tumor factors, iMac were co-cultured with 50% fresh supernatant from SK-MEL-28 cells every 24 h for 3 days. Supernatants were collected during the final 24 h for cytokine measurement. c Activation (phosphorylation) of NF-kB p65, STAT1, STAT3, and STAT6 in iMac was determined using Western blotting after conditioning with melanoma (SK-MEL-28) supernatant for 72 h. Protein band intensity was quantified using Odyssey version 3.0 software. After adjusting for loading using the β-actin band, data are presented as fold change to the iMac (Dox-) group, which is set as 1. For a – c , one-way ANOVA with Bonferroni’s correction for multiple comparisons was used to analyze group comparisons. Data are presented as means ± SD. Each experiment was performed three times, with triplicate samples each time. * p < 0.05, *** p < 0.001, and **** p < 0.0001

Article Snippet: The polyvinylidene difluoride (PVDF) membranes were incubated with specific primary antibodies against ACE (R&D Systems, MAB9291, 1:1,000), GAPDH (Sigma-Aldrich, SAB5600208, 1:2,000), β-actin (Sigma-Aldrich, A3854; 1:1000), phosphorylated NF-kB p65 (Novus, NB100-82086, 1:500), phosphorylated STAT1 (R&D Systems, AF2894, 1 μg/ml), phosphorylated STAT3 (Novus, NBP2-24463, 0.5 μg/ml), or phosphorylated STAT6 (Millipore, 06-937, 1:1000).

Techniques: Enzyme-linked Immunosorbent Assay, Cell Culture, Activation Assay, Phospho-proteomics, Western Blot, Software