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Journal: International Journal of Cardiology. Cardiovascular Risk and Prevention
Article Title: The sphingolipid metabolite sphingosine protects against hypertension by targeting metabolic-inflammatory crosstalk via the NLRP3 inflammasome
doi: 10.1016/j.ijcrp.2025.200562
Figure Lengend Snippet: SPH attenuates pathological changes and suppresses NLRP3 inflammasome activation in the hearts of hypertensive mice. (A, B) Masson's trichrome staining of heart (A) and aorta (B) sections, showing reduced collagen deposition (blue) with SPH treatment. Scale bars: 20 μm for heart, 50 μm (main) and 20 μm (inset) for aorta. (C) H&E staining of heart sections showing amelioration of myocardial disarray and inflammation. Scale bars: 500 μm (main) and 20 μm (inset).(D) ELISA quantification of serum IL-18 and IL-1β levels. Data are mean ± SEM. ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001, ∗∗∗∗P < 0.0001 vs. HBP group. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Article Snippet: Serum levels of interleukin-18 (IL-18) and interleukin-1β (IL-1β) were quantified using commercial
Techniques: Activation Assay, Staining, Enzyme-linked Immunosorbent Assay
Journal: International Journal of Cardiology. Cardiovascular Risk and Prevention
Article Title: The sphingolipid metabolite sphingosine protects against hypertension by targeting metabolic-inflammatory crosstalk via the NLRP3 inflammasome
doi: 10.1016/j.ijcrp.2025.200562
Figure Lengend Snippet: SPH mitigates Angiotensin II-induced inflammasome activation, apoptosis, and oxidative stress in HUVECs. (A, B) Representative immunofluorescence images showing increased expression of NLRP3 (red, A) and ASC (green, B) in AngII-treated cells, which is reduced by subsequent SPH treatment. Scale bar = 100 μm. (C) TUNEL assay (green) demonstrating increased apoptosis in AngII-treated cells, which is attenuated by SPH. Scale bar = 100 μm. (D, E) Biochemical assays showing that SPH or MCC950 treatment reverses the AngII-induced decrease in SOD1 activity (G).NO (H) and increase in MDA levels (D). (F, G) DCFH-DA staining showing increased intracellular ROS (green) after AngII treatment, which is suppressed by SPH or MCC950. Representative images (F) and quantification (E) are shown. (I, J) ELISA results showing that SPH or MCC950 treatment inhibits the AngII-induced secretion of IL-1β (I) and IL-18 (J). (K) Scanning electron microscopy (SEM) images showing that SPH or MCC950 treatment improves the cell surface morphology and reduces features of pyroptotic damage induced by AngII. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)
Article Snippet: Serum levels of interleukin-18 (IL-18) and interleukin-1β (IL-1β) were quantified using commercial
Techniques: Activation Assay, Immunofluorescence, Expressing, TUNEL Assay, Activity Assay, Staining, Enzyme-linked Immunosorbent Assay, Electron Microscopy
Journal: Neural Regeneration Research
Article Title: Sox2-overexpressing neural stem cells alleviate ventricular enlargement and neurological dysfunction in posthemorrhagic hydrocephalus
doi: 10.4103/NRR.NRR-D-24-01491
Figure Lengend Snippet: NSC Sox2 transplantation decreases the expression of proinflammatory factors and increases the expression of anti-inflammatory factors and neurotrophic factors in hippocampus. (A, B) ELISA results of TNF-α (A) and IL-1β (B) in hippocampus. (C) Typical western blot bands of TNF-α, IL-6, IL-10, BDNF, and NGF. (D) Statistical analysis of proteins. All data are presented as the mean ± SD ( n = 5). ** P < 0.01, *** P < 0.001, vs . Sham group (one-way analysis of variance followed by post hoc Tukey’s honestly significant difference test). BDNF: Brain-derived growth factor; ELISA: enzyme-linked immunosorbent assay; GAPDH: glyceraldehyde-3-phosphate dehydrogenase; IL: interleukin; IVH: intraventricular hemorrhage; NGF: nerve growth factor; NSC: neural stem cell; PBS: phosphate-buffered saline; SD: standard deviation; Sox2: sex-determining region Y-box 2; TNF-α: tumor necrosis factor-alpha.
Article Snippet: The supernatant was collected for the assay using
Techniques: Transplantation Assay, Expressing, Enzyme-linked Immunosorbent Assay, Western Blot, Derivative Assay, Saline, Standard Deviation
Journal: Journal of Advanced Research
Article Title: Natural, safety immunomodulatory derivatives of lactobacillus biofilms promote diabetic wound healing by metabolically regulating macrophage phenotype and alleviating local inflammation
doi: 10.1016/j.jare.2025.04.001
Figure Lengend Snippet: The effect of LBDs on JAK/STAT1 Signaling Pathway in vitro under JAK agonist (IL-6) stimulation. (a) Western blot analysis of JAK, STAT1 and pSTAT1 in the macrophage pro-treated with LPS. + IL-6 or + LBDs or co-treated. (b) Qualitative expression of CD206 + in the macrophage pro-treated with LPS. + IL-6 or + LBDs or co-treated. (c) IL-1β Enzyme-Linked Immunosorbent Assay (ELISA). (d) IL-6 Enzyme-Linked Immunosorbent Assay (ELISA). (e) IL-10 Enzyme-Linked Immunosorbent Assay (ELISA). (f) Cell migration status of different treatment groups at 24 h. (g) Quantitative representation of migration rate. (h) Cell proliferation of different treatment groups at 24 h.
Article Snippet: Translation: The protein expressions of IL-6, IL-1β, and IL-10 were detected using an
Techniques: In Vitro, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay, Migration
Journal: World Journal of Gastroenterology
Article Title: Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis via Bax/Bcl-2/caspase-3 signaling pathway
doi: 10.3748/wjg.v31.i47.113205
Figure Lengend Snippet: Impaired viability of islet β-cells in acute pancreatitis models. A-F: Cell Counting Kit-8 assay was used to assess the proliferation of islet β-cells (MIN-6) under control conditions, lipopolysaccharide stimulation (5 μg/mL or 10 μg/mL), and co-culture with media from lipopolysaccharide-treated 266-6 cells (A). Apoptosis in islet β-cells was evaluated in both acute pancreatitis cell and mouse models using the terminal deoxynucleotidyl transferase dUTP nick-end labeling assay (B and E). Quantitative analysis of terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive β-cells (C and F). Insulin secretion by islet β-cells in the acute pancreatitis model was quantified with an enzyme-linked immunosorbent assay kit (D). Representative results from three independent replicates are shown ( n = 8). a P < 0.05, b P < 0.01, c P < 0.001, d P < 0.0001. Data are presented as the mean ± SD. LPS: Lipopolysaccharide; AP: Acute pancreatitis; MAP: Mild acute pancreatitis; SAP: Severe acute pancreatitis; HE: Hematoxylin and eosin.
Article Snippet: The
Techniques: Cell Counting, Control, Co-Culture Assay, TUNEL Assay, Enzyme-linked Immunosorbent Assay
Journal: World Journal of Gastroenterology
Article Title: Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis via Bax/Bcl-2/caspase-3 signaling pathway
doi: 10.3748/wjg.v31.i47.113205
Figure Lengend Snippet: Tumor necrosis factor-α levels were elevated in acute pancreatitis models. A: Tumor necrosis factor-α levels in conditioned media from MIN-6 cells were quantified by enzyme-linked immunosorbent assay under control conditions, lipopolysaccharide stimulation (5 μg/mL or 10 μg/mL), and co-culture with media from lipopolysaccharide-treated 266-6 cells; B: Serum tumor necrosis factor-α levels in acute pancreatitis mouse models were quantified using the same methodology. Representative results from three independent replicates are shown. b P < 0.01, c P < 0.001, d P < 0.0001. Data are presented as the mean ± SD. AP: Acute pancreatitis; TNF-α: Tumor necrosis factor-α; LPS: Lipopolysaccharide; MAP: Mild acute pancreatitis; SAP: Severe acute pancreatitis.
Article Snippet: The
Techniques: Enzyme-linked Immunosorbent Assay, Control, Co-Culture Assay
Journal: World Journal of Gastroenterology
Article Title: Tumor necrosis factor-α promotes abnormal glucose metabolism after acute pancreatitis by inducing islet β-cell apoptosis via Bax/Bcl-2/caspase-3 signaling pathway
doi: 10.3748/wjg.v31.i47.113205
Figure Lengend Snippet: Inhibition of tumor necrosis factor-α expression attenuated the impairment of islet β-cell in acute pancreatitis models. A: Tumor necrosis factor-α levels in MIN-6 conditioned media were measured by enzyme-linked immunosorbent assay under control conditions, lipopolysaccharide stimulation (10 μg/mL), and co-culture with media from lipopolysaccharide-treated 266-6 cells, with or without treatment with a tumor necrosis factor-α inhibitor; B: Apoptosis was evaluated by terminal deoxynucleotidyl transferase dUTP nick-end labeling assay; C: Quantitative analysis of terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive β-cells; D: Insulin secretion by islet β-cells in the acute pancreatitis model was quantified using an enzyme-linked immunosorbent assay kit. Representative results from three independent replicate assays are shown. a P < 0.05, b P < 0.01, c P < 0.001, d P < 0.0001. Data are presented as the mean ± SD. AP: Acute pancreatitis; TNF-α: Tumor necrosis factor-α; LPS: Lipopolysaccharide.
Article Snippet: The
Techniques: Inhibition, Expressing, Enzyme-linked Immunosorbent Assay, Control, Co-Culture Assay, TUNEL Assay