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vdac inhibitor  (TargetMol)


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    Structured Review

    TargetMol vdac inhibitor
    <t>Inhibiting</t> <t>mPTP-VDAC</t> channel opening attenuates sevoflurane-induced mtDNA cytosolic escape and reduces cGAS-STING pathway activation in microglia. A BV2 cells were treated with 1 mM sevoflurane for 12 h after 1 µM CsA intervention for 30 min and 10 µM VBIT-4 intervention for 30 min. mtDNA levels of Nd1, Cytb, and D-loop in cytoplasm of BV2 cells were determined by real-time PCR ( n =3). B-I Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). J-Q Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). Data are expressed as the mean ± SD. Differences among multiple groups were performed using ANOVA. *P < 0.05, **P < 0.01, and ***P < 0.001.
    Vdac Inhibitor, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 7 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/vdac inhibitor/product/TargetMol
    Average 94 stars, based on 7 article reviews
    vdac inhibitor - by Bioz Stars, 2026-03
    94/100 stars

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    1) Product Images from "mtDNA-cGAS-STING axis-dependent NLRP3 inflammasome activation contributes to postoperative cognitive dysfunction induced by sevoflurane in mice"

    Article Title: mtDNA-cGAS-STING axis-dependent NLRP3 inflammasome activation contributes to postoperative cognitive dysfunction induced by sevoflurane in mice

    Journal: International Journal of Biological Sciences

    doi: 10.7150/ijbs.91543

    Inhibiting mPTP-VDAC channel opening attenuates sevoflurane-induced mtDNA cytosolic escape and reduces cGAS-STING pathway activation in microglia. A BV2 cells were treated with 1 mM sevoflurane for 12 h after 1 µM CsA intervention for 30 min and 10 µM VBIT-4 intervention for 30 min. mtDNA levels of Nd1, Cytb, and D-loop in cytoplasm of BV2 cells were determined by real-time PCR ( n =3). B-I Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). J-Q Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). Data are expressed as the mean ± SD. Differences among multiple groups were performed using ANOVA. *P < 0.05, **P < 0.01, and ***P < 0.001.
    Figure Legend Snippet: Inhibiting mPTP-VDAC channel opening attenuates sevoflurane-induced mtDNA cytosolic escape and reduces cGAS-STING pathway activation in microglia. A BV2 cells were treated with 1 mM sevoflurane for 12 h after 1 µM CsA intervention for 30 min and 10 µM VBIT-4 intervention for 30 min. mtDNA levels of Nd1, Cytb, and D-loop in cytoplasm of BV2 cells were determined by real-time PCR ( n =3). B-I Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). J-Q Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). Data are expressed as the mean ± SD. Differences among multiple groups were performed using ANOVA. *P < 0.05, **P < 0.01, and ***P < 0.001.

    Techniques Used: Activation Assay, Real-time Polymerase Chain Reaction, Western Blot

    Schematic illustration. Sevoflurane promoted DRP1-dependent mitochondrial fission to release mtDNA into the cytoplasm via the mPTP-VDAC channel, which induced the cGAS-STING pathway-dependent NLRP3 inflammasome activation, resulting in neuroinflammation of microglia.
    Figure Legend Snippet: Schematic illustration. Sevoflurane promoted DRP1-dependent mitochondrial fission to release mtDNA into the cytoplasm via the mPTP-VDAC channel, which induced the cGAS-STING pathway-dependent NLRP3 inflammasome activation, resulting in neuroinflammation of microglia.

    Techniques Used: Activation Assay



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    <t>Inhibiting</t> <t>mPTP-VDAC</t> channel opening attenuates sevoflurane-induced mtDNA cytosolic escape and reduces cGAS-STING pathway activation in microglia. A BV2 cells were treated with 1 mM sevoflurane for 12 h after 1 µM CsA intervention for 30 min and 10 µM VBIT-4 intervention for 30 min. mtDNA levels of Nd1, Cytb, and D-loop in cytoplasm of BV2 cells were determined by real-time PCR ( n =3). B-I Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). J-Q Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). Data are expressed as the mean ± SD. Differences among multiple groups were performed using ANOVA. *P < 0.05, **P < 0.01, and ***P < 0.001.
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    Image Search Results


    Inhibiting mPTP-VDAC channel opening attenuates sevoflurane-induced mtDNA cytosolic escape and reduces cGAS-STING pathway activation in microglia. A BV2 cells were treated with 1 mM sevoflurane for 12 h after 1 µM CsA intervention for 30 min and 10 µM VBIT-4 intervention for 30 min. mtDNA levels of Nd1, Cytb, and D-loop in cytoplasm of BV2 cells were determined by real-time PCR ( n =3). B-I Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). J-Q Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). Data are expressed as the mean ± SD. Differences among multiple groups were performed using ANOVA. *P < 0.05, **P < 0.01, and ***P < 0.001.

    Journal: International Journal of Biological Sciences

    Article Title: mtDNA-cGAS-STING axis-dependent NLRP3 inflammasome activation contributes to postoperative cognitive dysfunction induced by sevoflurane in mice

    doi: 10.7150/ijbs.91543

    Figure Lengend Snippet: Inhibiting mPTP-VDAC channel opening attenuates sevoflurane-induced mtDNA cytosolic escape and reduces cGAS-STING pathway activation in microglia. A BV2 cells were treated with 1 mM sevoflurane for 12 h after 1 µM CsA intervention for 30 min and 10 µM VBIT-4 intervention for 30 min. mtDNA levels of Nd1, Cytb, and D-loop in cytoplasm of BV2 cells were determined by real-time PCR ( n =3). B-I Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). J-Q Protein levels of NLRP3, pro-IL-1β, IL-1β p17, cGAS, STING, p-TBK1 Ser172 , and p-IRF3 Ser396 in the BV2 cells were detected by western blot ( n =3). Data are expressed as the mean ± SD. Differences among multiple groups were performed using ANOVA. *P < 0.05, **P < 0.01, and ***P < 0.001.

    Article Snippet: To evaluate the role of mitochondrial DNA in sevoflurane-induced inflammation in BV2 cells, we treated cells with the DRP1 inhibitor (Mdivi-1, 100 nM, MedChemExpress), the mPTP inhibitor (CsA, 1 µM, TargetMol, China) or the VDAC inhibitor (VBIT-4, 10 µM, TargetMol) 30 min before sevoflurane stimulation.

    Techniques: Activation Assay, Real-time Polymerase Chain Reaction, Western Blot

    Schematic illustration. Sevoflurane promoted DRP1-dependent mitochondrial fission to release mtDNA into the cytoplasm via the mPTP-VDAC channel, which induced the cGAS-STING pathway-dependent NLRP3 inflammasome activation, resulting in neuroinflammation of microglia.

    Journal: International Journal of Biological Sciences

    Article Title: mtDNA-cGAS-STING axis-dependent NLRP3 inflammasome activation contributes to postoperative cognitive dysfunction induced by sevoflurane in mice

    doi: 10.7150/ijbs.91543

    Figure Lengend Snippet: Schematic illustration. Sevoflurane promoted DRP1-dependent mitochondrial fission to release mtDNA into the cytoplasm via the mPTP-VDAC channel, which induced the cGAS-STING pathway-dependent NLRP3 inflammasome activation, resulting in neuroinflammation of microglia.

    Article Snippet: To evaluate the role of mitochondrial DNA in sevoflurane-induced inflammation in BV2 cells, we treated cells with the DRP1 inhibitor (Mdivi-1, 100 nM, MedChemExpress), the mPTP inhibitor (CsA, 1 µM, TargetMol, China) or the VDAC inhibitor (VBIT-4, 10 µM, TargetMol) 30 min before sevoflurane stimulation.

    Techniques: Activation Assay