vbit 4  (MedChemExpress)

Journal: Journal of Oral Microbiology

Article Title: P. gingivalis induces endothelial dysfunction via mitochondrial fission dependent VDAC1-HK2 disassociation

doi: 10.1080/20002297.2026.2643035

Figure Lengend Snippet: Drp1-dependent VDAC1 oligomerization is required for P. gingivalis induced mitochondrial dysfunction. HAECs was pretreated with or without Mdivi-1 (50 μM) and then infected with P. gingivalis for 24 h (MOI = 100). (A, B) Representative immunofluorescence images and statistics analysis showing the co-location of VDAC1 (red) and p -Drp1 (green) in HAECs. Scale bars: 20 μm (original) and 2 μm (Zoom). (C) The interaction of p -Drp1 and VDAC1 was validated using Co-immunoprecipitation assays. ( n = 3). (D, E) Immunoblot of VDAC1 cross-linking in HAECs pretreated with Mdivi-1 (50 μM) or VBIT-4 (20 μM) and quantitative analysis of oligomers. ( n = 3). (F, G) Calcein, MitoSOX staining assay and quantitative bar chart. Scale bars = 20 μm. ( n = 3) (H, I) Tube formation assay and quantitative bar chart. Scale bars = 200 μm. ( n = 3). Pg, P. gingivalis . All numbers ( n ) are biologically independent experiments. * P < 0.05. *** P < 0.001.

Article Snippet: Mdivi-1, the mPTP inhibitor cyclosporin A (CsA), and the VDAC1 oligomerization inhibitor VBIT-4 were purchased from TargetMol (USA).

Techniques: Infection, Immunofluorescence, Immunoprecipitation, Western Blot, Staining, Tube Formation Assay

Journal: Journal of Oral Microbiology

Article Title: P. gingivalis induces endothelial dysfunction via mitochondrial fission dependent VDAC1-HK2 disassociation

doi: 10.1080/20002297.2026.2643035

Figure Lengend Snippet: P. gingivalis triggers HK2 dissociation from VDAC1. HAECs were pretreated with Mdivi-1 (50 μM) or VBIT-4 (20 μM), followed by infection with P. gingivalis for 24 h. (MOI = 100). (A, B) Representative immunofluorescence images and statistics analysis showing the co-location of VDAC1 (red) and HK2 (green) in HAECs. Scale bars: 20 μm (original) and 5 μm (Zoom). (C) The interaction of VDAC1 and HK2 was validated using Co-immunoprecipitation assays. ( n = 3). (D, E) Representative immunoblots and quantification of HK2 levels in cytosolic and mitochondrial fractions of HAECs ( n = 3). (F, G) Representative immunofluorescence images and statistics analysis showing the co-location of mitochondria (red) and HK2 (green) in HAECs. Scale bars: 20 μm (original) and 5 μm (Zoom). ( n = 3). Pg, P. gingivalis . All numbers ( n ) are biologically independent experiments. ns = not significant. * P < 0.05. ** P < 0.01. *** P < 0.001.

Article Snippet: Mdivi-1, the mPTP inhibitor cyclosporin A (CsA), and the VDAC1 oligomerization inhibitor VBIT-4 were purchased from TargetMol (USA).

Techniques: Infection, Immunofluorescence, Immunoprecipitation, Western Blot

Journal: Advanced Science

Article Title: CypD Dependent mPTP Opening Is Crucial for Oxidized Mitochondrial DNA Release in Ferroptosis

doi: 10.1002/advs.202502239

Figure Lengend Snippet: OGG1 inhibition promotes ferroptosis via an mPTP‐dependent mechanism. (A) NCI‐H1299 cells were treated with increased doses of RSL3 as indicated in the presence of TH5487 (5 µ m ) and Fer‐1 (2 µ m ) for 8 h; then cell survival rate was measured by Cell Titer Glo Viability Assay. (B) The morphology of NCI‐H1299 cells treated with RSL3 (0.5 µ m ) for 4 h following TH5487 (5 µ m ) and Fer‐1 (2 µ m ) pre‐treatment. Scale bar was 50 µm. (C) NCI‐H1299 were treated with 5 µ m erastin as indicated in the presence of TH5487 (5 µ m ) and Ferrostatin (Fer‐1, 2 µ m ) for 18 h, and the lipid peroxidation level was determined using C11‐BODIPY staining by flow cytometry. (D) Quantitative analysis of the fold change of lipid oxidation ratio in (C). (E) GPX4 siRNA were transfected to HT‐1080 cells, after 36 h, TH5487, SU0268 and Fer‐1 were added as indicated, then cells viability was detected using Cell Titer Glo. (F) NCI‐H1299 were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without VBIT‐4 (5 µ m ) pretreatment for 8 h, then cell survival rate was measured by Cell Titer Glo Viability Assay. (G) NCI‐H1299 cells were treated with increased doses of erastin as indicated in the presence of TH5487 (5 µ m ), with or without CsA (5 µ m ) pretreatment for 24 h, and then the cell survival rate was measured by Cell Titer Glo Viability Assay. (H) CypD were knocked out in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. (I, J) ANT2 (I) and ANT3(J) were knocked down by specific siRNA in NCI‐H1299 cells, then the cells were treated with increased doses of erastin with or without TH5487 (5 µ m ) pretreatment. Cell death was measured by Cell Titer Glo Viability Assay. The statistical significance between different groups (D and E) was analyzed by Two‐Way ANOVA (Prism; GraphPad).

Article Snippet: RSL3 (T3646), erastin (T1765), ML210 (T8375), FINO2 ( T60084 ), CsA (T0945), DFO (T124358), BSO (T5471), TH5487 (T8119), SU0268 (T9119), Fer‐1 (T6500), VBIT‐4 ( T13287 ), H‐151 (T5674) and RU.521 (T5486) were ordered from TargetMol; Arachidonic acid (HY‐109590), Ardenic acid (HY‐W013215), and NIM811 (HY‐P0025) was purchased from MedChemExpress; IKE (MC2024) was purchased from MeilunBio.

Techniques: Inhibition, Viability Assay, Staining, Flow Cytometry, Transfection