anti ucp2  (Bioss)

Journal: Molecular Neurobiology

Article Title: B355252 Targets UCP2 to Rescue Intracerebral Hemorrhage-Induced Injury by Promoting Mitochondrial Fusion and Inhibiting Ferroptosis

doi: 10.1007/s12035-025-05368-5

Figure Lengend Snippet: B355252 targets UCP2 to suppress mitochondrial fission and oxidative stress. A , B Immunofluorescence staining confirms increased UCP2 levels in treated mice. C , D Western blot indicates that B355252 restores UCP2 expression within 24 h. E , F Molecular docking analysis shows strong binding between B355252 and UCP2. G , H 3D visualization highlights interaction residues. I , J Coronal brain sections revealed that UCP2-KO mice with ICH exhibited a significant increase in hemorrhage volume compared to the WT group. K – M Quantitative analysis of representative western blot bands, as well as the quantification of their grayscale values in the brain tissues of UCP2 knockout mice after B355252 treatment. N Cell viability assays demonstrated that the neuroprotective effect of B355252 was attenuated following Genipin treatment. O DHE staining confirmed that UCP2 knockdown attenuated the inhibitory effect of B355252 on ROS. P JC-1 staining demonstrated that UCP2 knockdown also reduced the protective effect of B355252 on mitochondrial membrane potential. (* p < 0.05, ** p < 0.01, *** p < 0.001)

Article Snippet: The membranes were blocked using 5% non-fat milk and probed overnight with primary antibodies, including FIS1 (1:5000, 10956–1-AP, Proteintech), MFN2 (1:5000, A19678, ABclonal), UCP2 (1:1000, 11081–1-AP, Proteintech), Ferritin (1:1000, 11682–1-AP, Proteintech), TFR1 (1:5000, 0084–2-AP, Proteintech), Gpx4 (1:4000, A1933, ABclonal), SLC7A11 (1:5000, 26864–1-AP, Proteintech), ACSL4 (1:4000, 22401–1-AP, Proteintech), and Tubulin (1:10000, 11224–1-AP, Proteintech).

Techniques: Immunofluorescence, Staining, Western Blot, Expressing, Binding Assay, Knock-Out, Knockdown, Membrane

Journal: Molecular Neurobiology

Article Title: B355252 Targets UCP2 to Rescue Intracerebral Hemorrhage-Induced Injury by Promoting Mitochondrial Fusion and Inhibiting Ferroptosis

doi: 10.1007/s12035-025-05368-5

Figure Lengend Snippet: B355252 reduces ICH-induced ferroptosis and oxidative stress in vivo and vitro. A – C Western blot shows decreased Ferritin and increased TFR1 in B355252-treated mice. D – G The results of oxidative stress markers (C11 BODIPY, GSH/GSSG, and MDA) indicate that Genipin inhibited the anti-oxidative stress effects of B355252. H – K Quantitative analysis of representative western blot bands, as well as the quantification of their grayscale values in the brain tissues of UCP2 knockout mice after B355252 treatment. L – O Y-maze and open field test indicated that the administration of an iron death inhibitor significantly reversed the impact of UCP2 knockdown on the neurological functions of mice with cerebral hemorrhage. ( n = 10). (* p < 0.05, ** p < 0.01, *** p < 0.001)

Article Snippet: The membranes were blocked using 5% non-fat milk and probed overnight with primary antibodies, including FIS1 (1:5000, 10956–1-AP, Proteintech), MFN2 (1:5000, A19678, ABclonal), UCP2 (1:1000, 11081–1-AP, Proteintech), Ferritin (1:1000, 11682–1-AP, Proteintech), TFR1 (1:5000, 0084–2-AP, Proteintech), Gpx4 (1:4000, A1933, ABclonal), SLC7A11 (1:5000, 26864–1-AP, Proteintech), ACSL4 (1:4000, 22401–1-AP, Proteintech), and Tubulin (1:10000, 11224–1-AP, Proteintech).

Techniques: In Vivo, Western Blot, Knock-Out, Knockdown

Journal: Molecular Neurobiology

Article Title: B355252 Targets UCP2 to Rescue Intracerebral Hemorrhage-Induced Injury by Promoting Mitochondrial Fusion and Inhibiting Ferroptosis

doi: 10.1007/s12035-025-05368-5

Figure Lengend Snippet: Therapeutic window and biosafety of B355252. A , B Protein blot analysis revealed temporal changes in UCP2 levels in mice with ICH following B355252 treatment. C In the in vitro model, B355252 rescues cell viability even when administered as late as 8.5 h post-treatment. D , E B355252 reduces hemorrhage volume and improves tissue integrity even when administered as late as 8.5 h post-ICH ( n = 10). F B355252 rescues brain water content even when administered as late as 8.5 h post-treatment. G , K Histopathological analysis of major organs shows no significant toxicity from B355252 ( n = 10). (* p < 0.05, ** p < 0.01, *** p < 0.001, n.s. stands for not significant)

Article Snippet: The membranes were blocked using 5% non-fat milk and probed overnight with primary antibodies, including FIS1 (1:5000, 10956–1-AP, Proteintech), MFN2 (1:5000, A19678, ABclonal), UCP2 (1:1000, 11081–1-AP, Proteintech), Ferritin (1:1000, 11682–1-AP, Proteintech), TFR1 (1:5000, 0084–2-AP, Proteintech), Gpx4 (1:4000, A1933, ABclonal), SLC7A11 (1:5000, 26864–1-AP, Proteintech), ACSL4 (1:4000, 22401–1-AP, Proteintech), and Tubulin (1:10000, 11224–1-AP, Proteintech).

Techniques: In Vitro

Journal: Molecular Neurobiology

Article Title: B355252 Targets UCP2 to Rescue Intracerebral Hemorrhage-Induced Injury by Promoting Mitochondrial Fusion and Inhibiting Ferroptosis

doi: 10.1007/s12035-025-05368-5

Figure Lengend Snippet: Schematic illustration of the potential mechanism of B355252 in alleviating intracerebral hemorrhage (ICH) in mice. ICH leads to decreased UCP2 expression, resulting in increased mitochondrial fission, increased reactive oxygen species (ROS), and ferroptosis. This study emphasizes B355252 targets UCP2 to promote mitochondrial fusion, mitigate ROS accumulation, and inhibit ferroptosis, thereby attenuating ICH-induced neuronal damage. Thus, B355252 may emerge as a new therapeutic strategy for the treatment of ICH

Article Snippet: The membranes were blocked using 5% non-fat milk and probed overnight with primary antibodies, including FIS1 (1:5000, 10956–1-AP, Proteintech), MFN2 (1:5000, A19678, ABclonal), UCP2 (1:1000, 11081–1-AP, Proteintech), Ferritin (1:1000, 11682–1-AP, Proteintech), TFR1 (1:5000, 0084–2-AP, Proteintech), Gpx4 (1:4000, A1933, ABclonal), SLC7A11 (1:5000, 26864–1-AP, Proteintech), ACSL4 (1:4000, 22401–1-AP, Proteintech), and Tubulin (1:10000, 11224–1-AP, Proteintech).

Techniques: Expressing