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1.
Fig. 1

Fig. 1. From: Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice.

Up-regulation of the Txnip gene after ischemic-reperfusion (I/R) injury. A real-time PCR-based array was performed to explore the overall changes in oxidative-related genes using samples of ischemic-damaged brains and sham brains (S). A) Among 84 genes, 38 were up-regulated and 46 gene transcripts were down-regulated 6 h after ischemic-reperfusion injury (n = 3). B) Among 46 genes, 17 were up-regulated over 1.5-fold compared with shams. These genes include Mpo, SOD3, NOX4, Txnip, and Ptgs2. C) Txnip mRNA was induced by 2.06-fold compared with sham controls (n = 3; *p = 0.026).

Gab Seok Kim, et al. Neurobiol Dis. ;46(2):440-449.
2.
Fig. 6

Fig. 6. From: Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice.

Knock-down of Txnip is neuroprotective after OGD in neurons. A) Txnip siRNA and scrambled siRNA were transfected with primary cortical neurons for 48 h. After transfection, the cells were harvested and the level of Txnip was analyzed by Western blotting. B) Forty-eight hours after siRNA transfection, the primary cortical neurons were subjected to OGD and allowed to reoxygenate for 20 h. The cell death rates were then measured by LDH assay (n = 6). *p < 0.05 compared with control without OGD and scrambled siRNA with OGD. C) Forty-eight hours after siRNA transfection, the primary cortical neurons were subjected to OGD and allowed to reoxygenate for 20 h. Cell viability was measured by WST assay (n = 6). *p < 0.05 compared with control without OGD and cells subjected to OGD. **p < 0.01 comparing Txnip siRNA#1-treated and untreated cells subjected to OGD. Scr, scrambled.

Gab Seok Kim, et al. Neurobiol Dis. ;46(2):440-449.
3.
Fig. 3

Fig. 3. From: Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice.

Oxidative stress can induce Txnip expression. A) Primary neuronal cells were exposed to OGD and allowed to reoxygenate for 1, 3, 6, and 24 h using glucose-free medium. Cells were harvested and analyzed by Western blotting to verify Txnip expression. β-tubulin was used as a loading control (n = 4). B) OGD and reoxygenation without glucose significantly increased Txnip in a time-dependent manner (n = 4; *p < 0.05). C) 3-NP was injected into the striatum of brains using a stereotactic apparatus, and the damaged striatum was collected 3, 6, and 24 h after the injection. Western blot was preformed to detect Txnip. β-tubulin was used as a loading control (n = 4). D) 3-NP administration to the brains resulted in an increase in Txnip 6 and 24 h after injection (n = 4; *p < 0.05). O.D., optical density; Veh, vehicle.

Gab Seok Kim, et al. Neurobiol Dis. ;46(2):440-449.
4.
Fig. 4

Fig. 4. From: Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice.

Calcium is important for induction of Txnip after oxidative stress. A) Primary neuronal cells treated with various concentrations of 2-APB were exposed to OGD and allowed to reoxygenate for 6 and 24 h using glucose-free medium. Western blot analysis was performed to confirm the level of Txnip. β-tubulin was used as a loading control (n = 4). B) This graph shows the dramatic reduction in Txnip by 2-APB after OGD and reoxygenation (n = 4; *p < 0.01). C) Primary neuronal cells treated with various concentrations of diltiazem were exposed to OGD and allowed to reoxygenate for 24 h using medium without glucose. Western blot analysis was performed to verify the level of Txnip. GAPDH was used as a loading control (n = 4). D) Primary neuronal cells were treated with 50 μM verapamil, exposed to OGD, and allowed to reoxygenate for 24 h using glucose-free medium. Western blotting was performed to confirm the level of Txnip. GAPDH was used as a loading control (n = 4). E) Treatment with diltiazem and verapamil in primary neurons subjected to OGD and reoxygenation showed a great reduction in Txnip in a dose-dependent manner (n = 4; p < 0.05). O.D., optical density.

Gab Seok Kim, et al. Neurobiol Dis. ;46(2):440-449.
5.
Fig. 2

Fig. 2. From: Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice.

Txnip is induced by ischemic-reperfusion (I/R) injury in mice. Transient cerebral ischemia was induced by MCAO and the brains were isolated at various times after reperfusion. A) Western blot analysis was performed using sham (S) samples 1, 3, 6, 12, and 24 h after I/R with a Txnip antibody. β-tubulin was used as a loading control (n = 6). B) This graph shows that Txnip expression was enhanced 3, 6, 12, and 24 h after ischemic brain injury compared with the sham controls (n = 6; *p < 0.05). C) Immunofluorescence images show that Txnip-positive cells were increased by I/R injury (n = 4). Scale bar: 50 μm. D) Txnip-positive cells were colocalized with NeuN, a neuronal cell marker. Scale bar: 50 μm. E) Confocal images show that Txnip is located in the cytoplasm of neurons. Scale bar: 10 μm. O.D., optical density; DAPI, 4′,6 diamidino-2-phenylindole.

Gab Seok Kim, et al. Neurobiol Dis. ;46(2):440-449.
6.
Fig. 5

Fig. 5. From: Induction of thioredoxin-interacting protein is mediated by oxidative stress, calcium, and glucose after brain injury in mice.

Txnip mRNA induction is mediated by oxidative stress and glucose. A) A hyperglycemic-ischemia animal model was used, along with a single dose (240 mg/kg) of STZ injected intraperitoneally. Three days after the injection, the glucose level was confirmed with a OneTouch Ultra device using blood from a tail snip. Ischemic injury was then induced by 30 min of MCAO and reperfusion was induced by removal of the suture. Blood glucose levels were verified right before and after MCAO (n = 10). p < 0.01 compared with normoglycemia. B) Mice with normal blood glucose levels induced by citrate buffer or with high glucose levels induced by STZ were subjected to 30 min of MCAO by insertion of a suture. Brains were collected at 3, 6, and 24 h after reperfusion. Western blotting with an anti-3-nitrotyrosine (3-NT) and anti-β-tubulin antibody was performed to confirm ROS production after hyperglycemic ischemia (n = 4). C) Infarction volume was measured by 2,3,5-triphenyltetrazolium chloride staining using slices from the brains of normoglycemic-ischemic or hyperglycemic-ischemic brains 6 h after reperfusion (normoglycemic-ischemic, n = 5; hyperglycemic-ischemic, n = 6; *p < 0.05). D) Overall gene expression profiles induced by hyperglycemic stress and ischemic-reperfusion injury (n = 3). E) Genes up-regulated by glucose over 1.5-fold included Ccs, Txnip, Gpx1, and Ucp3 (hyperglycemic shams vs. normoglycemic shams). F) Genes up-regulated over 1.5-fold included Noxo1, Il19, Nos2, Txnip, and Zmynd17 (hyperglycemic-ischemic reperfusion for 6 h vs. normoglycemic-ischemic reperfusion for 6 h). G) Genes up-regulated over 1.5-fold included Mpo, Xirp1, Ptgs2, SOD3, Txnip, and Il19 (hyperglycemic-ischemic reperfusion for 6 h vs. hyperglycemic shams). H) Changes in Txnip mRNA after ischemic-reperfusion injury in hyperglycemic or normoglycemic mice (n = 3, *p < 0.05 compared with normoglycemic-ischemic reperfusion for 6 h and hyperglycemic shams). conc., concentration; NG, normoglycemic; I/R, ischemic-reperfusion; HG, hyperglycemic; S, sham.

Gab Seok Kim, et al. Neurobiol Dis. ;46(2):440-449.

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