Journal: Frontiers in Pharmacology

Article Title: Dexmedetomidine alleviates lung ischemia-reperfusion injury by inhibiting cuproptosis: an in vivo study

doi: 10.3389/fphar.2025.1562535

Figure Lengend Snippet: WB results of cuproptosis-related protein expression. (A) Western blots for FDX 1, SLC 31 A1, LIAS, DLST, DLD, and SDHB in rat lung tissue. (B–G) relative levels of FDX 1, SLC 31 A1, LIAS, DLST, DLD, and SDHB in rat lung tissue (n = 3). ## p < 0.05 vs. control group; ** p < 0.05 vs. I/R group.

Article Snippet: Membranes were incubated overnight at 4°C with primary antibodies against: lipoic acid (Abcam, 1:1,000), FDX1 (Abcam, 1:1,000), LIAS (Proteintech, 1:1,000), SDHB (Proteintech, 1:1,000), DLAT (Proteintech, 1:1,000), DLD (Proteintech, 1:1,000), SLC31A1 (MCE, 1:1,000), DLST (MCE, 1:1,000), and β-actin (Sevier, 1:5,000).

Techniques: Expressing, Western Blot, Control

Journal: Frontiers in Pharmacology

Article Title: Dexmedetomidine alleviates lung ischemia-reperfusion injury by inhibiting cuproptosis: an in vivo study

doi: 10.3389/fphar.2025.1562535

Figure Lengend Snippet: Immunohistochemical and WB results of lipoacylated proteins. (A–C) representative images of lipoacylated protein immunohistochemical staining in rat lung tissue. (D) Western blots for lip-DLAT and lip-DLST. (E, F) relative levels of lip-DLAT and lip-DLST in rats lung tissue (n = 3). ## p < 0.05 vs. control group; ** p < 0.05 vs. I/R group.

Article Snippet: Membranes were incubated overnight at 4°C with primary antibodies against: lipoic acid (Abcam, 1:1,000), FDX1 (Abcam, 1:1,000), LIAS (Proteintech, 1:1,000), SDHB (Proteintech, 1:1,000), DLAT (Proteintech, 1:1,000), DLD (Proteintech, 1:1,000), SLC31A1 (MCE, 1:1,000), DLST (MCE, 1:1,000), and β-actin (Sevier, 1:5,000).

Techniques: Immunohistochemical staining, Staining, Western Blot, Control

Journal: Cell Reports

Article Title: A lncRNA-mediated metabolic rewiring of cell senescence

doi: 10.1016/j.celrep.2025.115747

Figure Lengend Snippet: sin-lncRNA interacts with DLST and controls its subcellular localization (A) RNA-FISH based on locked nucleic acid (LNA) technology on fixed IMR90 ER:RAS cells depleted or not of sin-lncRNA (siRNA_sin-lncRNA#1/3) and treated for 5 days with 4OHT. Two different LNAs were used. Incubation without LNA probe (“No_probe”) was used as control. Scale bar: 10 μm. (B) RT-qPCR analysis of a set of genes after mitochondria purification from proliferating (−4OHT) or senescent cells (+4OHT) using Mitotracker (green, 488) staining and FACS sorter. The graph shows a representative experiment. (C) Schematic representation of the TCA cycle that takes place in the mitochondria. DLST enzyme is highlighted in red. (D) RNA immunoprecipitation analysis monitoring DLST binding to sin-lncRNA, MALAT1 , and GAPDH RNA in control and sin-lncRNA -depleted (siRNA#1/3) senescent IMR90 ER:RAS, using anti-DLST antibody or IgG as a negative control. The graph represents the mean ± SD ( n = 2). (E) Left, western blot analysis of DLST cellular fractionation in control and sin-lncRNA -depleted (siRNA#1/3) senescent IMR90 ER:RAS. GAPDH and H3 were used as cytoplasmic and nuclear controls, respectively. Right, percentage of nuclear and cytoplasmic distribution of DLST normalized to GAPDH (cyto) or H3 (nucl). The graph represents the mean ± SD ( n = 3). Two-tailed Student’s t test, ∗ ∗ p < 0.01.

Article Snippet: After centrifugation, the samples were precleared with Dynabeads Protein A (Invitrogen) for 1 h. One per cent of the sample was used as the input control and the remaining extracts were incubated with 10 μg DLST antibody (Bethyl) or IgG at 4 °C overnight.

Techniques: Incubation, Control, Quantitative RT-PCR, Purification, Staining, RNA Immunoprecipitation, Binding Assay, Negative Control, Western Blot, Cell Fractionation, Two Tailed Test