Journal: Molecular Medicine Reports

Article Title: Prenatal lipopolysaccharide exposure programs cardiac fibrosis via dysregulating of connexin 43 in offspring rats

doi: 10.3892/mmr.2026.13830

Figure Lengend Snippet: BW of offspring rats from 1-day to 16-week-old (A). Heart damages in offspring at the age of 8 and 16 weeks, including the ratios (B) LVW/BW, (C) HW/BW and (D) NT-proBNP level in serum. Concentration of Ang II in (E) left ventricle and (F) serum. Data are presented as mean ± SD. n=10 in each group (A-C) and n=7 in each group (D-F). *P<0.05, **P<0.01 vs Con. BW, body weight; HW, heart weight; LVW, left ventricular weight; NT-proBNP, N-terminal pro-brain natriuretic peptide; Ang II, angiotensin II; Con, control; LPS, lipopolysaccharide.

Article Snippet: Serum concentrations of N-terminal pro-BNP (NT-proBNP; cat. no. E-EL-R3023) and Ang II, along with myocardial tissue levels of Ang II (cat. no. E-EL-R1430c), were quantified using commercial ELISA kits (Elabscience Biotechnology Co., Ltd.) following manufacturer protocols.

Techniques: Concentration Assay, Control

Journal: Cardio-oncology

Article Title: Macrophage surface protein Mac-2 mediates inflammatory and stromal stress pathways in doxorubicin-induced cardiac injury

doi: 10.1186/s40959-026-00443-9

Figure Lengend Snippet: Galectin-3 (Mac-2) regulates DOX uptake, macrophage activation, and downstream stress signaling in vitro. a Flow cytometry showing increased percentages of Mac-2 + RAW 264.7 macrophages after 24-hour treatment with 0.1 µM, 0.5 µM, and 1 µM DOX ( p < 0.01; n = 6–9). b Schematic of CRISPR/Cas9-mediated Lgals3 (Mac-2) knockout in RAW 264.7 macrophages targeting exon 3 with specific guide RNAs. Fluorescence microscopy and flow cytometry confirming efficient transfection with 86% (8600/10000) co-expression of RFP and GFP in knockout cells, scale bars: 50 μm. c Flow cytometry histograms quantifying % DOX⁺ macrophages in WT and Mac-2 KO cells after 24 h DOX treatment (0.1–1 µM). Mac-2 KO macrophages show significantly reduced DOX uptake at every concentration tested ( p < 0.001; n = 4–8). d Flow cytometry quantification of % marker⁺ macrophages (CCR2, F4/80, MHC-II) after 24 h of 0.1 µM DOX. Mac-2 KO cells display significantly lower CCR2⁺, F4/80⁺, and MHC-II⁺ populations compared with WT ( p < 0.001; n = 8). e IL-6-induced chemotactic migration is significantly increased in WT macrophages compared to KO cells ( p < 0.001; n = 8). f Relative mRNA levels of pro-inflammatory (M1) genes ( Ccl2 , Il6 , Tnf ) increase with DOX in WT macrophages but are attenuated in KO; n = 6–9. (* represents p = 0.05; n = 6–9). g Anti-inflammatory (M2) markers ( Il10 , Cd206 , Arg1 ) are reduced in WT macrophages after DOX but partially restored in KO. h Lysosomal/Autophagy signaling genes ( Tfeb , Lamp1 , Map1lc3b , Sqstm1 were altered in WT macrophages following DOX, but normalized or rescued in KO ( p = 0.05 ). i Macrophage-mediated caspase-3/7 activation in cardiomyocytes (CMs): CMs were either treated directly with DOX or co-cultured with WT or KO macrophages (± DOX). The “indirect” condition refers to CMs cultured with pre-DOX-treated macrophages (0.1 µM, 24 h), without direct drug exposure. Caspase-3/7 activation is increased in CMs co-cultured with DOX-treated WT macrophages but not KO macrophages ( p < 0.0001). j Phospho-TFEB (Ser211) ELISA in cardiac fibroblasts co-cultured with macrophages shows increased activation with DOX-treated WT macrophages, suppressed with KO macrophages ( p < 0.01). DOX, doxorubicin; KO, Mac-2 knockout; WT-C, wild-type controls; KO-C, knockout controls, CMC, cardiomyocytes; CFC, cardiac fibroblasts

Article Snippet: Serum BNP levels were measured using a Mouse/Rat BNP ELISA Kit (RayBiotech, EIAM-BNP-1).

Techniques: Activation Assay, In Vitro, Flow Cytometry, CRISPR, Knock-Out, Fluorescence, Microscopy, Transfection, Expressing, Concentration Assay, Migration, Cell Culture, Enzyme-linked Immunosorbent Assay