Journal: Medicine

Article Title: Triptolide combined with arsenic trioxide induces apoptosis of myelodysplastic syndrome cells by inhibiting the NF-κB signaling pathway

doi: 10.1097/MD.0000000000046206

Figure Lengend Snippet: Effects of TL and ATO alone or in combination inhibits NF- κB signaling pathway. (A) The expression of canonical NF-κB pathways (IkBα and p65) mRNA and related proteins in SKM-1 cells treated with TL (30 ng/mL), ATO (8 μmol/L), TL and ATO (30 ng/mL + 8 μmol/L) in combination by RT-qPCR (n = 3) and Western Blotting. (B) The expression non-canonical NF-κB pathways (p52 and RelB) mRNA and related protein in SKM-1 cells treated with TL (30 ng/mL), ATO (8 μmol/L), TL and ATO (30 ng/mL + 8 μmol/L) in combination by RT-qPCR (n = 3) and Western Blotting. Compared with the blank control group,* P < .05, ** P < .01, *** P < .001, **** P < .0001, ns = no significance. Compared with the TL or ATO alone group, # P < .05, ## P < .01, ### P < .001.

Article Snippet: Western blot, qPCR, and BCA protein assay kits were obtained from Nanjing Vazyme Biotech Co., Ltd. Antibodies targeting apoptosis proteins like Bcl-2, Bcl-XL, cIAP1, Caspase-3, Caspase-8, and poly ADP-ribose polymerase (PARP), as well as those for NF-κB pathway proteins including IkBα, p65, p52, and RelB, were obtained from Proteintech Group, Inc.

Techniques: Expressing, Quantitative RT-PCR, Western Blot, Control

Journal: Medicine

Article Title: Triptolide combined with arsenic trioxide induces apoptosis of myelodysplastic syndrome cells by inhibiting the NF-κB signaling pathway

doi: 10.1097/MD.0000000000046206

Figure Lengend Snippet: Schematic presentation indicating the suggested mechanisms by which inhibit NF-κB-induced SKM-1 cell apoptosis by ATO combined with TL. The combined effect of TL and ATO inhibits the NF-κB signaling pathway, promotes the expression of p65, further inhibits the expression of IkBα, p52, and RelB, further upregulates the expression of Caspase-3, Caspase-8, PARP, downregulates the expression of Bcl-2, Bcl-XL, and cIAP1, and ultimately promotes SKM-1 cell apoptosis.

Article Snippet: Western blot, qPCR, and BCA protein assay kits were obtained from Nanjing Vazyme Biotech Co., Ltd. Antibodies targeting apoptosis proteins like Bcl-2, Bcl-XL, cIAP1, Caspase-3, Caspase-8, and poly ADP-ribose polymerase (PARP), as well as those for NF-κB pathway proteins including IkBα, p65, p52, and RelB, were obtained from Proteintech Group, Inc.

Techniques: Expressing

Journal: bioRxiv

Article Title: Self-Reactive B Cells in Artery Tertiary Lymphoid Organs Encode Pathogenic High Affinity Autoantibody in Atherosclerosis

doi: 10.1101/2025.07.10.664251

Figure Lengend Snippet: (A) Relative composition of six B cell subtypes was determined based on their transcript profiles as shown in Figure S1; scRNA-seq identified six B cell subsets in each tissue according to their transcript profiles: naїve B cells, newly activated B cells (Nac B cells), early GC B cells, late GC B cells, memB cells and PCs; percentages of each B cell subtype in each tissue is indicated by different colors in the circle plots; the total number of B cells analyzed per tissue is shown in the inner circle. Statistical analysis was performed using the Chi-square test with Benjamini-Hochberg correction. (B) Selected transcripts in individual B cell subsets; Violin plots show B cell activation (Nfkbia, Relb), migration (CXCR4), the B cell inhibitory checkpoint (CD22) gene expression profiles in B cell subsets in different tissues. Each dot represents one single B cell. Statistical analysis was performed using the Kruskal-Wallis H Test with Benjamini-Hochberg correction. (C) Quantitative immunofluorescent analyses of key regulatory molecule-expressing cells in WT and Apoe -/- RLNs and ATLOs; immunofluorescence followed by morphometry of CXCR4 + B cells and RelB + B cells but lower numbers of BCL6 + B cells in B cell areas. Tissue sections were stained using anti-CXCR4, anti-RelB, anti-BCL6 and anti-B220 antibodies. Quantification of the number of positive cells/area per section of CXCR4 + B cells (migratory B cells), RelB + B cells (activated B cells), and BCL6 + B cells (follicular B cells) within B220 + B cell areas were determined as described in Methods. Bars 100 μm. Each dot represents one field; 5-6 fields per mouse per tissue, n = 5 WT RLNs, 5 Apoe -/- RLNs, and 5 ATLOs from 5 Apoe -/- mice. (D) Number of somatic hypermutations (SHM) per BCR heavy chain; each dot represents one B cell. P values of two-group comparisons were determined by the Wilcoxon Rank Sum Test. (E) Pie charts show distinct ATLO traits of clonally expanded vs non-expanded B cell subtypes; sizes of circles represent the relative cell numbers within each tissue; blue indicates the percentage of clonally expanded B cells within each subset. (F) Percentages of class-switched BCRs in different B cell subsets WT and Apoe -/- RLNs vs ATLOs; sizes of circles represent the relative cell numbers within each tissue; blue indicates the percentages of class switched B cell subtypes; G-H, Chi-square test with Benjamini-Hochberg correction was used to perform statistical analyses;

Article Snippet: Immunofluorescence staining was performed using ATLO GC- derived, RLN GC-derived antibodies, anti-mouse CD11c (N418, Serotec), alpha smooth muscle actin (SMA, 1A4, SIGMA), CXCR4(UMB2, Abcam), RelB (C-19, Santa Cruz Biotechnology), CD35 (8C12, Biosciences), and BCL6 (K112-91, Biosciences).

Techniques: Activation Assay, Migration, Gene Expression, Expressing, Immunofluorescence, Staining