Journal: Neural Regeneration Research

Article Title: High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury

doi: 10.4103/NRR.NRR-D-23-01772

Figure Lengend Snippet: Experimental groups

Article Snippet: C57BL/6 mice were randomly divided into five groups: (1) Control group, which underwent the surgical procedures but without TBI; (2) TBI group, which received saline for 3 days; (3) TBI + DEX group (Sigma–Aldrich, D4902), which was administered an intraperitoneal injection once per day for 3 days; (4) DEX+RU486 (Abcam, Cambridge, UK, Cat# ab120356), which received a GR antagonist, RU486, twice a day for 1 day before TBI and 3 days after surgery; administration of DEX was consistent with group (3); and (5) RU486 + ruxolitinib group (TargetMol, Wellesley Hills, MA, USA, Cat# 1,092,939-17-7), which received RU486 as in group (4) , while the Janus kinase (JAK) inhibitor, ruxolitinib, was administered twice daily for three days post-TBI (Lescoat et al., 2020; Chen et al., 2021).

Techniques: Control, Saline, Western Blot, TUNEL Assay, Staining, Immunofluorescence

Journal: Neural Regeneration Research

Article Title: High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury

doi: 10.4103/NRR.NRR-D-23-01772

Figure Lengend Snippet: RU486 and ruxolitinib treatment decreases DEX-induced apoptosis following TBI. (A, B) Representative photomicrographs (A) and quantification (B) of terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining. Apoptotic cells were measured in the ipsilateral hippocampus and cortex surrounding the injury site. Green represents TUNEL-positive cells. Blue represents DAPI. Scale bars: 20 μm. Data are expressed as mean ± SD, n = 3. * P < 0.05, vs . Control; # P < 0.05, vs. traumatic brain injury (TBI) (one-way analysis of variance with the least significant difference test). DAPI: 4′,6-Diamidino-2-phenylindole; DEX: dexamethasone; TBI: traumatic brain injury.

Article Snippet: C57BL/6 mice were randomly divided into five groups: (1) Control group, which underwent the surgical procedures but without TBI; (2) TBI group, which received saline for 3 days; (3) TBI + DEX group (Sigma–Aldrich, D4902), which was administered an intraperitoneal injection once per day for 3 days; (4) DEX+RU486 (Abcam, Cambridge, UK, Cat# ab120356), which received a GR antagonist, RU486, twice a day for 1 day before TBI and 3 days after surgery; administration of DEX was consistent with group (3); and (5) RU486 + ruxolitinib group (TargetMol, Wellesley Hills, MA, USA, Cat# 1,092,939-17-7), which received RU486 as in group (4) , while the Janus kinase (JAK) inhibitor, ruxolitinib, was administered twice daily for three days post-TBI (Lescoat et al., 2020; Chen et al., 2021).

Techniques: TUNEL Assay, Staining, Control

Journal: Neural Regeneration Research

Article Title: High-dose dexamethasone regulates microglial polarization via the GR/JAK1/STAT3 signaling pathway after traumatic brain injury

doi: 10.4103/NRR.NRR-D-23-01772

Figure Lengend Snippet: Inhibition of GR attenuates neuronal death. (A) Representative image of Nissl staining in the peri-injured cortex and hippocampus. (B) Quantification analysis showed that DEX induced a significant decrease in Nissl-positive cells post-TBI. RU486 application alleviated neuronal loss. Scale bars: 20 μm. Data are expressed as mean ± SD, n = 3. * P < 0.05, vs . Control; # P < 0.05, vs. TBI (one-way analysis of variance with the least significant difference test). DEX: Dexamethasone; TBI: traumatic brain injury.

Article Snippet: C57BL/6 mice were randomly divided into five groups: (1) Control group, which underwent the surgical procedures but without TBI; (2) TBI group, which received saline for 3 days; (3) TBI + DEX group (Sigma–Aldrich, D4902), which was administered an intraperitoneal injection once per day for 3 days; (4) DEX+RU486 (Abcam, Cambridge, UK, Cat# ab120356), which received a GR antagonist, RU486, twice a day for 1 day before TBI and 3 days after surgery; administration of DEX was consistent with group (3); and (5) RU486 + ruxolitinib group (TargetMol, Wellesley Hills, MA, USA, Cat# 1,092,939-17-7), which received RU486 as in group (4) , while the Janus kinase (JAK) inhibitor, ruxolitinib, was administered twice daily for three days post-TBI (Lescoat et al., 2020; Chen et al., 2021).

Techniques: Inhibition, Staining, Control

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: Stress induces corticosterone-mediated CD8 + T cell exhaustion to promote non-small cell lung cancer

doi: 10.1007/s00262-025-04179-w

Figure Lengend Snippet: Corticosterone (COR) promotes CD8 + T cell exhaustion and NSCLC growth. a The LLC tumor growth curves and the endpoint tumor weights were displayed of control (Con) and corticosterone treatment (COR) mice (n = 5). (b-d) Flow cytometric analysis of the proportions of PD-1 + and LAG3 + , granzyme B + and IFN-γ + of CD8 + T cells of tumor tissues from Con and COR mice (n = 4). (e-f) The LLC tumor growth curves, the endpoint tumor weights and tumor sizes were showed of acute restraint (AR+PBS) and acute restraint+RU486 treatment (AR+RU486) mice (n = 6). g CCK-8 detection of CD8 + T cell viability after 24 hours of treatment with different concentrations of COR. Flow cytometric analysis of the proportions of h IFN-γ + , i granzyme B + , j LAG3 + , k PD-1 + and l TIM-3 + of CD8 + T cells among DMSO, COR and COR+RU486 treatment groups (n = 3). Data are represented as the mean ± standard error of the mean (SEM). * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001 by an unpaired Student’s T-test or one-way ANOVA

Article Snippet: At the same time, mice exposure to RU486 were treated glucocorticoid receptor (GR) inhibitors RU486 once a day (i.p. 10mg/kg) (HY-13683, MedChemExpress).

Techniques: Control, CCK-8 Assay

Journal: Cancer Immunology, Immunotherapy : CII

Article Title: Stress induces corticosterone-mediated CD8 + T cell exhaustion to promote non-small cell lung cancer

doi: 10.1007/s00262-025-04179-w

Figure Lengend Snippet: Smart RNA sequencing reveals the mechanism of stress regulated CD8 + T cell function. a Isolation process of CD8 + T cells from mice tumors. b Differential genes of CD8 + T cells in tumors of the control (Con) and acute stress (AR) mice (n = 3) (|Log 2 (Fold change)| ≥ 1 and p < 0.05). c KEGG analysis of differential genes of CD8 + T cells and the most significant 20 enriched pathways are displayed ( p < 0.05). d GSEA analysis of differential genes of CD8 + T cells and the most significant 20 enriched pathways are displayed ( p < 0.05). Detect the mRNA expression levels of Plcg1 e , Prkcq f , Tec g , Grap2 h , Rasgrp1 i , Ppp3cc j , Mapk11 k and Mapk14 l in CD8 + T cells among DMSO, COR and COR+RU486 treatment groups using qRT-PCR (n = 3). Data are represented as the mean ± standard error of the mean (SEM). * p < 0.05, ** p < 0.01, *** p < 0.001 and **** p < 0.0001 by one-way ANOVA e – l

Article Snippet: At the same time, mice exposure to RU486 were treated glucocorticoid receptor (GR) inhibitors RU486 once a day (i.p. 10mg/kg) (HY-13683, MedChemExpress).

Techniques: RNA Sequencing, Cell Function Assay, Isolation, Control, Expressing, Quantitative RT-PCR