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