Journal: BMC Medicine

Article Title: Therapeutic activation of PPARα contributes to NOTCH1 inhibition in T-cell acute lymphoblastic leukemia

doi: 10.1186/s12916-026-05045-x

Figure Lengend Snippet: Chiglitazar activates PPARα and exerts cytotoxic effects on T-ALL cell lines in vitro. ( A ) Western blot analysis showing that chiglitazar treatment dose-dependently enhances PPARα protein expression in Jurkat and Molt4 cells, without significantly affecting PPARγ levels. ( B - C ) CCK-8 assay ( B ) and trypan blue staining ( C ) showing the viability and proliferation of Jurkat and Molt4 cells treated with increasing concentrations of chiglitazar at 24, 48, and 72 h, indicating dose- and time-dependent inhibition. ( D ) EdU incorporation assays confirming significantly reduced cell proliferation in Jurkat and Molt4 cells following 24 h of chiglitazar treatment. ( E ) Flow cytometry analysis of the cell cycle revealing that chiglitazar treatment for 24 h induces G0/G1 phase arrest in T-ALL cells. ( F ) Colony formation assays showing a significant reduction in the colony-forming ability of Jurkat and Molt4 cells treated with indicated concentrations of chiglitazar and cultured for 14 days. (G-H) Flow cytometry analysis using Annexin V/PI staining demonstrates that chiglitazar treatment for 24 h induces apoptosis in Jurkat and Molt4 cells in a dose-dependent manner. Data are presented as mean ± SD (* p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001)

Article Snippet: The following primary antibodies were used: PPARα (Abcam); PPARγ (ABclonal); GAPDH (HUABIO); NOTCH1 (Abcam); NICD (Cell Signaling Technology); RPBJK (Abcam); Hes1 (Cell Signaling Technology); Hey1 (ABclonal); Bcl-2 (Cell Signaling Technology); Bcl-XL (Cell Signaling Technology); C-Myc (Cell Signaling Technology); STAT3 (Cell Signaling Technology); p-STAT3 (Cell Signaling Technology); Lamin B1 (Cell Signaling Technology); β-Tubulin (Proteintech).

Techniques: In Vitro, Western Blot, Analysis, Expressing, CCK-8 Assay, Staining, Inhibition, EdU Assay, Flow Cytometry, Colony Assay, Cell Culture

Journal: Pharmaceuticals

Article Title: Physical Exercise Enhances Melatonin Effect in D-Galactose/Aluminum Chloride-Induced Alzheimer’s Disease of Ovariectomized Rats: Irisin Induction Associated with Upregulation of PPAR-γ/IGF-1/BDNF and Decreasing TNF-α/p38-MAPK/NLRP3/GFAP Pathway

doi: 10.3390/ph19050770

Figure Lengend Snippet: Effects of MTN (10 mg/kg/day; i.p.) and PHE, alone or in combination, on PPAR-γ protein expression and IGF-1 content in OVX/AD rats. ( A ) Photomicrographs of the hippocampus subiculum sections immunostained with PPAR-γ, scale bar = 50 μm (200×) (black arrows represent the number of positive neurons of hippocampal PPAR-γ). ( B ) Number of positive neurons of hippocampal PPAR-γ, and ( C ) hippocampal content of IGF-1. Data are presented as mean ± SD ( n = 4 and 6 for PPAR-γ and IGF-1, respectively). Statistical analysis was conducted by GraphPad Prism, one-way ANOVA followed by Tukey–Kramer as a post hoc test for multiple comparison; (***) p ≤ 0.001, (****) p ≤ 0.0001. Correlation analysis was performed using Pearson’s correlation coefficient. AD: Alzheimer’s disease; ANOVA: analysis of variance; IGF-1: insulin growth factor; MTN: melatonin; OVX: ovariectomized; PPAR-γ: peroxisome proliferator-activated receptor gamma; PHE: physical exercise.

Article Snippet: Four 4 μm thick formalin-fixed paraffin slices of hippocampi were prepared and incubated for immunostaining according to the procedures of [ , ] for the subsequent primary antibodies: Aβ, 1:100 (ABClonal, Woburn, MA, USA, Cat No: A17911); PPAR-γ, 1:100 dilution (ABClonal, Woburn, MA, USA, Cat No: A0270); and BDNF, 1:100 dilution (Servicebio, Wuhan, China, Cat No: GB11559).

Techniques: Expressing, Comparison

Journal: iScience

Article Title: Deletion of miR-130b/301b cluster promotes macrophage efferocytosis and resolution of adipose tissue inflammation

doi: 10.1016/j.isci.2026.115307

Figure Lengend Snippet: miR-130b inhibits macrophage expression of PGC-1α and PPARγ protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).

Article Snippet: The blots were incubated with antibodies specific for PPARγ (Cell Signaling Technology, #2435), PGC-1α (Cell Signaling Technology, #4259), β-actin (Cell Signaling Technology, #5125), CX3CR1 (Abcam, ab308613), and GAPDH (Proteintech, 60004), and detected by enhanced chemiluminescence (Pierce).

Techniques: Expressing, Derivative Assay, Transfection, Negative Control, Isolation, Knock-Out, Incubation, Cell Culture

Journal: iScience

Article Title: Deletion of miR-130b/301b cluster promotes macrophage efferocytosis and resolution of adipose tissue inflammation

doi: 10.1016/j.isci.2026.115307

Figure Lengend Snippet: miR-130b inhibits macrophage expression of PGC-1α and PPARγ protein (A) Sequences of PPAR and PGC-1 3′-UTR targeted by miR-130b-3p and miR-301b-3p. (B) Bone marrow-derived macrophages (BMDMs) were transfected with miR-130b-3p mimics, miR-301b-3p mimics, or negative control (con). Total proteins were subjected for WB analysis at 2 days after transfection. Blots and quantifications of PGC-1α and PPARγ proteins (normalized to GAPDH of the same blot) were shown. (C) BMDMs were isolated from WT and miR-130b/301B knockout mice (KO) and incubated with apoptotic thymocytes. After engulfment for 6 h, the cells were replaced with fresh medium and cultured for 2 days before collection for WB analysis. WB blots and quantifications of PGC-1α and PPARγ proteins (normalized to βactin from same blot) were shown. Bar graphs were shown as mean ± SD, n = 3–4 cell samples, ∗ p < 0.05; ∗∗ p < 0.01 ( t test for B; ANOVA for C).

Article Snippet: The blots were incubated with antibodies specific for PPARγ (Cell Signaling Technology, #2435), PGC-1α (Cell Signaling Technology, #4259), β-actin (Cell Signaling Technology, #5125), CX3CR1 (Abcam, ab308613), and GAPDH (Proteintech, 60004), and detected by enhanced chemiluminescence (Pierce).

Techniques: Expressing, Derivative Assay, Transfection, Negative Control, Isolation, Knock-Out, Incubation, Cell Culture