cleaved c  (Quidel)

Journal: Journal of Neuroinflammation

Article Title: iPLA2β-dependent phospholipid remodeling drives ZIKV-induced neuroinflammation and neurological injury

doi: 10.1186/s12974-026-03973-2

Figure Lengend Snippet: iPLA2β deficiency alleviates ZIKV-induced neuropathology and neuroinflammation. A Survival of neonatal iPLA2β −/− and WT mice following intracerebroventricular infection with ZIKV was monitored throughout the experimental period. n = 10. B Clinical scores of ZIKV-infected iPLA2β −/− and WT mice were evaluated longitudinally during the infection. n = 10. C Body weight changes in ZIKV-infected iPLA2β −/− and WT mice were measured longitudinally. n = 10. D Brain weights of ZIKV-infected iPLA2β −/− and WT mice at 7 dpi. n = 15. E ZIKV RNA levels in the cortex of ZIKV-infected iPLA2β −/− and WT mice at 5 and 7 dpi. n = 10. F Colocalization of ZIKV E protein and NeuN-positive neurons in the cortex of ZIKV-infected mice at 7 dpi, as shown by representative immunofluorescence images. Scale bar, 100 μm. n = 6. G Protein levels of cleaved caspase-3 in the prefrontal cortex of ZIKV-infected iPLA2β −/− and WT mice at 7 dpi. n = 3. H Neuronal loss and glial activation in the cortex of ZIKV-infected iPLA2β−/− and WT mice at 7 dpi, as shown by representative NeuN, Iba1, and GFAP immunostaining images. Scale bar, 100 μm. n = 6. I mRNA expression levels of the pro-inflammatory cytokines Tnf-α , Il-6 , and Il-1β in the cortex of ZIKV-infected iPLA2β −/− and WT mice at 7 dpi. n = 6. J PGE₂ levels in the cortex of ZIKV-infected iPLA2β −/− and WT mice at 7 dpi. n = 8. Data are presented as mean ± SEM. Statistical significance was assessed using the Mann–Whitney U test for (B–C, G, I–J) and one-way ANOVA followed by Tukey’s multiple-comparison test for (E, H). * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: Primary antibodies used included anti-ZIKV NS5 (1:1000, GeneTex, GTX133312), anti-ZIKV E protein (1:1000, GeneTex, GTX133314), anti-iPLA2β (1:1000, Santa Cruz, sc-376563), anti-Myc (1:1000, CST, #5605), anti-cleaved caspase-3 (1:1000, CST, #9661), and anti-β-actin (1:5000, Proteintech, USA).

Techniques: Infection, Immunofluorescence, Activation Assay, Immunostaining, Expressing, MANN-WHITNEY, Comparison

Journal: Journal of Neuroinflammation

Article Title: iPLA2β-dependent phospholipid remodeling drives ZIKV-induced neuroinflammation and neurological injury

doi: 10.1186/s12974-026-03973-2

Figure Lengend Snippet: Targeting iPLA2β-mediated lipid dysregulation attenuates ZIKV infection and associated neuroinflammation. A Experimental design showing neonatal mice intracerebroventricularly infected with ZIKV and subsequently treated with FKGK18, PE-DHA, or their combination. B Survival of ZIKV-infected mice following treatment with FKGK18, PE-DHA, or combined treatment was monitored throughout the experimental period. n = 10. C Brain weights of ZIKV-infected iPLA2β-/- and WT mice at 7 dpi. n = 15. D ZIKV RNA levels in the cortex of ZIKV-infected mice at 5 and 7 dpi following treatment with FKGK18, PE-DHA, or their combination. n = 10. E Neuronal preservation and glial activation in the cortex of ZIKV-infected mice following the indicated treatments at 7 dpi, as shown by representative NeuN, GFAP, and CD68/Iba1 immunofluorescence images. Scale bar, 100 μm. n = 6. F Ca²⁺-independent phospholipase A2 activity in primary cortical neurons at 48 h post-infection (hpi). n = 6. G ZIKV E protein levels in primary cortical neurons at 48 hpi under the indicated treatment conditions. H Protein levels of cleaved caspase-3 in primary cortical neurons at 48 hpi under the indicated treatment conditions. n = 3. I Protein levels of the pro-inflammatory cytokines TNF-α, IL-6, and IL-1β in primary cortical neurons at 48 hpi, as determined by ELISA. n = 6. Data are presented as mean ± SEM. Statistical significance was assessed using one-way ANOVA followed by Tukey’s multiple-comparison test. * p < 0.05, ** p < 0.01, *** p < 0.001

Article Snippet: Primary antibodies used included anti-ZIKV NS5 (1:1000, GeneTex, GTX133312), anti-ZIKV E protein (1:1000, GeneTex, GTX133314), anti-iPLA2β (1:1000, Santa Cruz, sc-376563), anti-Myc (1:1000, CST, #5605), anti-cleaved caspase-3 (1:1000, CST, #9661), and anti-β-actin (1:5000, Proteintech, USA).

Techniques: Infection, Preserving, Activation Assay, Immunofluorescence, Activity Assay, Enzyme-linked Immunosorbent Assay, Comparison

Journal: Molecular Therapy Oncology

Article Title: Trabectedin decreases myeloid resistance to improve the efficacy of anti-PD1 immunotherapy and delay glioma malignant progression

doi: 10.1016/j.omton.2026.201147

Figure Lengend Snippet: Combination trabectedin and anti-PD1 ICB prolongs survival of glioma-bearing mice (A) Schematic depicting the treatment regimen for the Ntv-a x XFM-luc RCAS murine glioma progression model. Four groups of mice were treated with vehicle, trabectedin (2 doses, 1 week apart, starting at week 4), anti-PD-1 immune checkpoint blockade (ICB; 3 doses, 3 days apart, starting at week 3.5), or a combination of trabectedin and anti-PD-1 ICB. (B) Kaplan-Meier survival analysis of the four treatment groups. Vehicle ( n = 12), anti-PD1 ( n = 8), trabectedin ( n = 13), and trabectedin + anti-PD1 ( n = 12) had median survivals of 39, 43, 43, and 53 days, respectively. Significance was determined using the log-rank (Mantel-Cox) test ( p < 0.0001∗∗∗∗, p < 0.0002 ∗∗∗, p < 0.0021∗∗, p < 0.0332∗). (C) Representative images of cleaved caspase-3 (c-cas3) immunohistochemical (IHC) staining of tumors isolated from glioma-bearing mice 3 days post treatment 2 (3DPT2) with vehicle, trabectedin, or trabectedin + anti-PD1 combination. (D) Quantification of c-cas3 IHC staining. Positive pixels were calculated by sampling 5 equal-sized regions within each tumor core and comparing the number of positive pixels per region ( n = 2–5 mice per treatment group). Significance was determined using a paired t test with Welch’s correction ( p < 0.0005∗∗∗∗, p < 0.005 ∗∗∗, p < 0.005∗∗, p < 0.05∗). Error bars show SD.

Article Snippet: Slides were washed in TBST and stained with c-cas3 (R&D Systems MAB835, Minneapolis, MN) at a 1:100 dilution for 2 h at room temperature.

Techniques: Immunohistochemical staining, Immunohistochemistry, Isolation, Sampling