Journal: iScience

Article Title: Comparative effects of semaglutide tirzepatide and retatrutide on renal fibrosis in UUO and aged mice

doi: 10.1016/j.isci.2026.117174

Figure Lengend Snippet: Semaglutide, tirzepatide, and retatrutide alleviate renal fibrosis in aged by modulating the G2/M phase (A–C) KEGG pathway enrichment plots of semaglutide, tirzepatide, and retatrutide groups versus the aged group ( n = 3). (D) Clustered heatmap ( n = 3). (E–G) CRE levels in the semaglutide, tirzepatide, and retatrutide groups before and after inhibitor treatment ( n = 6). (H) WB analysis of Collagen III, α-SMA, Cyclin B1, and CDK1 protein expression levels in renal tissues of each group before and after inhibitor treatment ( n = 3). Data are represented as mean ± SEM, significant differences were determined by one way ANOVA followed by Tukey’s post hoc test; n , the number of independent biological replicates, ∗ p < 0.05.

Article Snippet: Cyclin B1 , ABclonal , Cat#A19037; RRID: AB_2862529.

Techniques: Expressing

Journal: iScience

Article Title: Comparative effects of semaglutide tirzepatide and retatrutide on renal fibrosis in UUO and aged mice

doi: 10.1016/j.isci.2026.117174

Figure Lengend Snippet: Semaglutide, tirzepatide, and retatrutide inhibit the increase in fibrotic levels induced by senescence in HK-2 cells (A) β-galactosidase staining. Scale bars, 50 μm. (B) Flow cytometric analysis of HK-2 cell cycle. (C) WB detection of the expression of Collagen III, α-SMA, Cyclin B1 and CDK1 in HK-2 cells. (D)Statistical graphs of WB analysis showing Collagen III, α-SMA, Cyclin B1, and CDK1 expression in HK-2 cells across experimental groups before and after inhibitor treatment. Data are represented as mean ± SEM, one-way ANOVA followed by Tukey’s post hoc test was used for comparisons involving five or more groups; n = 3; n , the number of independent biological replicates; ∗ p < 0.05.

Article Snippet: Cyclin B1 , ABclonal , Cat#A19037; RRID: AB_2862529.

Techniques: Staining, Expressing

Journal: iScience

Article Title: Comparative effects of semaglutide tirzepatide and retatrutide on renal fibrosis in UUO and aged mice

doi: 10.1016/j.isci.2026.117174

Figure Lengend Snippet:

Article Snippet: Cyclin B1 , ABclonal , Cat#A19037; RRID: AB_2862529.

Techniques: Recombinant, Staining, Enzyme-linked Immunosorbent Assay, SYBR Green Assay, RNA Sequencing, Sequencing, Software

Journal: Materials Today Bio

Article Title: Low-toxicity vitrification of small-diameter arterial grafts by achieving a Cryo-Stasis state

doi: 10.1016/j.mtbio.2026.103439

Figure Lengend Snippet: CTX-Rads stabilizes the nuclear envelope via Lamin B1 to inhibit cell death. (A) Immunofluorescence staining of Lamin B1 in HUVECs after exposure to CPAs for the indicated durations. Cells were fixed with 4% paraformaldehyde without unloading. (B) Lamin B1 mean fluorescence intensity was quantified from (A) ( n ≥ 30 cells per group). (C) HUVECs were transfected with Lamin B1 overexpression plasmid (OE) or empty vector (Control) (n = 3). For (C – E), transfected cells were subjected to VS55 loading (exposure for 15 min) followed by one-step unloading. DNA damage was assessed by γ -H2AX immunofluorescence. Representative images are shown in panel C, and the percentage of γ -H2AX positive cells is quantified in (D). UT, untreated. (E) Cell viability of Lamin B1-overexpressing HUVECs was measured by CCK-8 assay (n = 3). (F, G) HUVECs were subjected to Lamin B1 knockdown. These cells were then exposed to CTX-Rads loading (exposure for 60 min or 90 min) followed by one-step unloading. DNA damage was evaluated in (F) and cell viability in (G) (n = 3). (H) CTX-Rads upregulates Lamin B1 to stabilize the nucleus and enhance cell survival during unloading, whereas VS55 compromises this protective mechanism. All experiments was performed in triplicate. Data: mean ± SD; Tukey’s test: ns, P > 0.05 ; * P ≤ 0.05 , ** P ≤ 0.01 , *** P ≤ 0.001 .

Article Snippet: They were then incubated with a rabbit anti-lamin B1 primary antibody (ABclonal, A1910; 1:200) followed by an Alexa FluorTM 488-conjugated goat anti-rabbit IgG secondary antibody (Thermo Fisher, Cat# A11034; 1:500).

Techniques: Immunofluorescence, Staining, Fluorescence, Transfection, Over Expression, Plasmid Preparation, Control, CCK-8 Assay, Knockdown

Journal: Journal of Translational Medicine

Article Title: Tumor-derived progranulin promotes macrophage cholesterol efflux and associated immunosuppressive features in oral squamous cell carcinoma

doi: 10.1186/s12967-026-08422-5

Figure Lengend Snippet: Tumor-derived PGRN regulates macrophage cholesterol efflux through the PPARγ-LXRα-ABCA1/ABCG1 axis. A-B. mRNA ( A ) and protein ( B ) expression levels of PPARγ, LXRα, ABCA1, ABCG1, and SR-B1 in THP-1 macrophages cultured with HIOEC-CM or CAL27-CM. C-D. Suppression of these cholesterol efflux regulators in macrophages cultured with shPGRN-CAL27-CM compared with shNC-CAL27-CM. E-F. Effects of the PGRN-SORT1 interaction inhibitor (HY-115213, 2 µM) on CAL27-CM-induced activation of the PPARγ-LXRα-ABCA1/ABCG1 axis. G-H. Restoration of PPARγ, LXRα, ABCA1, and ABCG1 expression in PGRN-deficient systems (shPGRN-CAL27-CM) following PPARγ activation with rosiglitazone (RSG). I-J. Intracellular and extracellular cholesterol levels in THP-1 ( I ) and RAW264.7 ( J ) macrophages cultured with shPGRN-CAL27-CM, with or without RSG treatment. K. Filipin III staining of RAW264.7 macrophages showing intracellular cholesterol changes under the same conditions, with corresponding semi-quantitative MFI analysis. Representative images are shown at 200× (upper panels) and 400× (lower panels) magnification. Quantitative data are from n = 3 independent experiments per group unless otherwise indicated; panels I and J: n = 4 per group. Panel K MFI was quantified from six randomly selected fields per condition. *, p < 0.05; **, p < 0.01; ***, p < 0.001; ****, p < 0.0001; ns, not significant

Article Snippet: Membranes were blocked and then incubated with primary antibodies against PGRN (1:500, 10826-RP03, Sino Biological, Beijing, China), ABCA1 (1:1000, #96292, Cell Signaling Technology, MA, USA), ABCG1 (1:1000, A17907, ABclonal, Wuhan, China), SR-B1 (1:800, A0827, ABclonal, Wuhan, China), PPARγ (1:2500, 16643-1-AP, Proteintech, Wuhan, China), LXRα (1:5000, 14351-1-AP, Proteintech, Wuhan, China), and GAPDH (1:20,000, 10494-1-AP, Proteintech, Wuhan, China).

Techniques: Derivative Assay, Expressing, Cell Culture, Activation Assay, Staining