Journal: Journal of Inflammation Research

Article Title: TXNIP Participated in NLRP3-Mediated Inflammation in a Rat Model of Cervical Spondylotic Myelopathy

doi: 10.2147/JIR.S373614

Figure Lengend Snippet: The expression of TNXIP in the lesioned spinal cord following compression was observed. ( A ) The TNXIP/NeuN expression in the anterior horn of lesioned spinal cords was analyzed by immunofluorescence. The mean fluorescence intensities of TXNIP were analyzed by Image J software, and represented as mean gray values. ( B ) The TXNIP expression in the lesioned spinal cords was analyzed by Western blot. The gray values of protein bands were analyzed by Image J software, and protein expression was normalized to GAPDH. *P<0.05, **P<0.01.

Article Snippet: The primary antibodies included rabbit anti-rat TXNIP (1:800, MA5-32771, ThermoFisher), NLRP3 (1:800, MA5-32255, ThermoFisher), pro-caspase-1 (1:800, MA5-35833, ThermoFisher) and GAPDH (1:10000, PA1-16777, ThermoFisher).

Techniques: Expressing, Immunofluorescence, Fluorescence, Software, Western Blot

Journal: Journal of Inflammation Research

Article Title: TXNIP Participated in NLRP3-Mediated Inflammation in a Rat Model of Cervical Spondylotic Myelopathy

doi: 10.2147/JIR.S373614

Figure Lengend Snippet: Inhibition of TXNIP improved CSM-induced behavioral deficits. ( A ) The21-point Basso, Beattie and Bresnahan (BBB) locomotor rating scale; ( B ) cold allodynia; ( C ) inclined plane test. Compared with the sham group, **P<0.01; compared with the scrambled group, # P<0.05, ## P<0.01.

Article Snippet: The primary antibodies included rabbit anti-rat TXNIP (1:800, MA5-32771, ThermoFisher), NLRP3 (1:800, MA5-32255, ThermoFisher), pro-caspase-1 (1:800, MA5-35833, ThermoFisher) and GAPDH (1:10000, PA1-16777, ThermoFisher).

Techniques: Inhibition

Journal: Journal of Inflammation Research

Article Title: TXNIP Participated in NLRP3-Mediated Inflammation in a Rat Model of Cervical Spondylotic Myelopathy

doi: 10.2147/JIR.S373614

Figure Lengend Snippet: Inhibition of TXNIP reduced apoptosis in the anterior horn of the lesioned area following CSM. ( A ) Positive TUNEL staining control. ( B ) Apoptosis in the anterior horn of the lesioned area was analyzed by TUNEL staining. Black arrows show apoptotic cells. Apoptosis rate (%) = the numbers of apoptosis cells/total numbers of cells ×100%. The numbers of cells were counted using Image J software. Compared with the sham group, **P<0.01; compared with the scrambled group, ## P<0.01.

Article Snippet: The primary antibodies included rabbit anti-rat TXNIP (1:800, MA5-32771, ThermoFisher), NLRP3 (1:800, MA5-32255, ThermoFisher), pro-caspase-1 (1:800, MA5-35833, ThermoFisher) and GAPDH (1:10000, PA1-16777, ThermoFisher).

Techniques: Inhibition, TUNEL Assay, Staining, Control, Software

Journal: Journal of Inflammation Research

Article Title: TXNIP Participated in NLRP3-Mediated Inflammation in a Rat Model of Cervical Spondylotic Myelopathy

doi: 10.2147/JIR.S373614

Figure Lengend Snippet: Inhibition of TXNIP declined the TXNIP expression in the anterior horn of the lesioned area following CSM. The mean fluorescence intensities of TXNIP/NeuN were analyzed by immunofluorescence. The mean gray values were analyzed using Image J software. Compared with the sham group, *P<0.05, **P<0.01; compared with the scrambled group, ## P<0.01.

Article Snippet: The primary antibodies included rabbit anti-rat TXNIP (1:800, MA5-32771, ThermoFisher), NLRP3 (1:800, MA5-32255, ThermoFisher), pro-caspase-1 (1:800, MA5-35833, ThermoFisher) and GAPDH (1:10000, PA1-16777, ThermoFisher).

Techniques: Inhibition, Expressing, Fluorescence, Immunofluorescence, Software

Journal: Journal of Inflammation Research

Article Title: TXNIP Participated in NLRP3-Mediated Inflammation in a Rat Model of Cervical Spondylotic Myelopathy

doi: 10.2147/JIR.S373614

Figure Lengend Snippet: Inhibition of TXNIP declined the NLRP3 expression in the anterior horn of the lesioned area following CSM. The mean fluorescence intensities of NLRP3/NeuN were analyzed by immunofluorescence. The mean gray values were analyzed by Image J software. Compared with the sham group, **P<0.01; compared with the scrambled group, ## P<0.01.

Article Snippet: The primary antibodies included rabbit anti-rat TXNIP (1:800, MA5-32771, ThermoFisher), NLRP3 (1:800, MA5-32255, ThermoFisher), pro-caspase-1 (1:800, MA5-35833, ThermoFisher) and GAPDH (1:10000, PA1-16777, ThermoFisher).

Techniques: Inhibition, Expressing, Fluorescence, Immunofluorescence, Software

Journal: Journal of Inflammation Research

Article Title: TXNIP Participated in NLRP3-Mediated Inflammation in a Rat Model of Cervical Spondylotic Myelopathy

doi: 10.2147/JIR.S373614

Figure Lengend Snippet: Inhibition TXNIP declined the NLRP3 mediated pro-caspase-1 expression in the anterior horn of the lesioned area following CSM. ( A ) The mean fluorescence intensities of pro-caspase-1/NeuN were analyzed by immunofluorescence. ( B ) The expression levels of TXNIP, NLRP3 and pro-caspase-1 in the lesioned spinal cords were measured by Western blot. The mean grays were analyzed by the Image J software. Compared with the sham group, **P<0.01; compared with the scrambled group, ## P<0.01.

Article Snippet: The primary antibodies included rabbit anti-rat TXNIP (1:800, MA5-32771, ThermoFisher), NLRP3 (1:800, MA5-32255, ThermoFisher), pro-caspase-1 (1:800, MA5-35833, ThermoFisher) and GAPDH (1:10000, PA1-16777, ThermoFisher).

Techniques: Inhibition, Expressing, Fluorescence, Immunofluorescence, Western Blot, Software

Journal: Journal of Alzheimer's Disease

Article Title: Thioredoxin-Interacting Protein (TXNIP) Associated NLRP3 Inflammasome Activation in Human Alzheimer’s Disease Brain

doi: 10.3233/jad-180814

Figure Lengend Snippet: Fig. 1. TXNIP transcription, expression, and co-localization in cortices of postmortem human AD brains. Frontal and temporal cortical samples were collected from AD and non-AD brains and were subjected to TXNIP analysis. Immunoblotting analysis on frontal specimens revealed a significant (∗p < 0.05) increase in TXNIP expression in AD brains compared to non-AD counterparts (A). The mRNA levels also significantly (∗∗∗p < 0.001) increased in AD brains, as compared to non-AD brains (B). TXNIP was then examined for co-localization with A or p-tau within the temporal cortices of AD brains as a hallmark of AD pathology (C). Sections were immunostained with anti-A and anti-TXNIP antibodies respectively. Representative images display higher expression and co-localization of A (green) and TXNIP (red) in AD compared to non-AD brain (a-b). Separate sections were also immunostained for p-tau and TXNIP demonstrating higher expression and co-localization of TXNIP (green) and p-tau ser262 (red) in AD compared to non-AD brains (c-d). Boxed area shows the enlarged view of co-localization of TXNIP with A and p-tau. The arrow indicates the immunopositive signals for TXNIP. Scale bar = 50 m. Labeled intensity and labeled positive area also significantly increased in AD brains, as compared to non-AD brains (D). The arrow indicates the immunopositive signals for TXNIP. Values are expressed as median ± SD for TXNIP signal intensity and mean ± SD for other bars.

Article Snippet: The 180 membranes were blocked for non-specific bind- 181 ing and probed with primary antibodies against 182 TXNIP (1:1000; NBP1-5 4578, Novus Biologicals), 183 TRX (1:1000; C63C6, Cell Signaling Technology), 184 NLRP3, cleaved caspase-1, ASC (1:1000; AG-20B- 185 0014; AG-20B-0042; AG-25B-0006, Adipogen Life 186 Sciences), pro-IL-1 or cleaved IL-1 (1:1000; 187 ab9722; Abcam, USA) at 4◦C overnight.

Techniques: Expressing, Western Blot, Labeling

Journal: Journal of Alzheimer's Disease

Article Title: Thioredoxin-Interacting Protein (TXNIP) Associated NLRP3 Inflammasome Activation in Human Alzheimer’s Disease Brain

doi: 10.3233/jad-180814

Figure Lengend Snippet: Fig. 5. Schematic description of presumable link between TXNIP and AD pathology. TXNIP co-localization with A plaques or p-tau in temporal cortices of Alzheimer’s disease (AD) patients suggest a causative link between TXNIP and AD pathology. As determined by dotted arrows it is not yet clear whether the pathological aggregates may boost TXNIP expression or TXNIP precedes A or tau buildup. TXNIP activity has an established role to propagate oxidative stress and inflammation. Through direct binding to TRX, TXNIP impedes TRX radical scavenging activity. Recently, TXNIP has been found to interact with NLRP3 inflam- masome and improve its cleavage activity to cleave precursors of capase-1 and IL-1. IL-1 over-expression in the vicinity of A aggregates suggest a prior activation of the NLRP3 inflamma- some induced by either TXNIP overexpression or aggregated A itself. TXNIP, thioredoxin interacting protein; TRX, thioredoxin; A, amyloid- protein; p-tau, phosphorylated tau protein; ASC, apoptosis-associated speck-like protein; Cas-1, caspase-1; IL-1, interleukine-1.

Article Snippet: The 180 membranes were blocked for non-specific bind- 181 ing and probed with primary antibodies against 182 TXNIP (1:1000; NBP1-5 4578, Novus Biologicals), 183 TRX (1:1000; C63C6, Cell Signaling Technology), 184 NLRP3, cleaved caspase-1, ASC (1:1000; AG-20B- 185 0014; AG-20B-0042; AG-25B-0006, Adipogen Life 186 Sciences), pro-IL-1 or cleaved IL-1 (1:1000; 187 ab9722; Abcam, USA) at 4◦C overnight.

Techniques: Expressing, Activity Assay, Binding Assay, Over Expression, Activation Assay

Journal: BioMed Research International

Article Title: Effects of Hypoxic Environment on Periodontal Tissue through the ROS/TXNIP/NLRP3 Inflammasome Pathway

doi: 10.1155/2022/7690960

Figure Lengend Snippet:

Article Snippet: Membranes were blocked with 5% skimmed milk in TBST for 1 h at room temperature and then incubated with the following primary antibodies overnight at 4°C: TXNIP (Rabbit IgG, Boster, China), NLRP3 (Rabbit IgG, Boster, China), ASC (Rabbit IgG, Immunoway, China), and caspase-1 (Rabbit IgG, Immunoway, China) at 1 : 1000.

Techniques:

Journal: BioMed Research International

Article Title: Effects of Hypoxic Environment on Periodontal Tissue through the ROS/TXNIP/NLRP3 Inflammasome Pathway

doi: 10.1155/2022/7690960

Figure Lengend Snippet: Effects of systemic hypoxia stimulation on the expression of TXNIP/NLRP3 signaling pathway-related factors in periodontal tissues of rats: (a) immunofluorescence staining (IF) showed that TXNIP, NLRP3, ASC, and caspase-1 in periodontal tissues. Ab: alveolar; PL: periodontal ligament; R: root. Scale bars = 25 μ m. (b) RT-PCR analysis of TXNIP, NLRP3, ASC, caspase-1, and IL-1 β in periodontal tissues ( n = 5). (c) Western blotting analysis of TXNIP, NLRP3, ASC, caspase-1, and IL-1 β in periodontal tissues ( n = 5 for each group). The above data are presented as the mean ± SEM, ∗ p < 0.05.

Article Snippet: Membranes were blocked with 5% skimmed milk in TBST for 1 h at room temperature and then incubated with the following primary antibodies overnight at 4°C: TXNIP (Rabbit IgG, Boster, China), NLRP3 (Rabbit IgG, Boster, China), ASC (Rabbit IgG, Immunoway, China), and caspase-1 (Rabbit IgG, Immunoway, China) at 1 : 1000.

Techniques: Expressing, Immunofluorescence, Staining, Reverse Transcription Polymerase Chain Reaction, Western Blot

Journal: BioMed Research International

Article Title: Effects of Hypoxic Environment on Periodontal Tissue through the ROS/TXNIP/NLRP3 Inflammasome Pathway

doi: 10.1155/2022/7690960

Figure Lengend Snippet: Hypoxic environment induced by CoCl 2 activates the ROS/TXNIP/NLRP3 inflammasome pathway in periodontal membrane fibroblasts. (a) Effects of different concentrations of CoCl 2 on the proliferation of periodontal membrane fibroblasts cultured for 24 h and 48 h. (b, c) Immunofluorescence staining (IF) showed that the expressions of ROS, TXNIP, NLRP3, ASC, and caspase-1 were in the cells treated with different concentrations of CoCl 2. . Scale bars = 1 μ m. (d) RT-PCR analysis of TXNIP, NLRP3, caspase-1, ASC, and IL-1 β in HPDLCs cells treated with 200 μ M and 400 μ M CoCl 2 for 24 h. (e) Western blotting analysis of TXNIP, NLRP3, caspase-1, ASC, and IL-1 β in HPDLC cells treated with 200 μ M and 400 μ M for 24 h. The above data are presented as the mean ± SEM, ∗ p < 0.05.

Article Snippet: Membranes were blocked with 5% skimmed milk in TBST for 1 h at room temperature and then incubated with the following primary antibodies overnight at 4°C: TXNIP (Rabbit IgG, Boster, China), NLRP3 (Rabbit IgG, Boster, China), ASC (Rabbit IgG, Immunoway, China), and caspase-1 (Rabbit IgG, Immunoway, China) at 1 : 1000.

Techniques: Membrane, Cell Culture, Immunofluorescence, Staining, Reverse Transcription Polymerase Chain Reaction, Western Blot

Journal: BioMed Research International

Article Title: Effects of Hypoxic Environment on Periodontal Tissue through the ROS/TXNIP/NLRP3 Inflammasome Pathway

doi: 10.1155/2022/7690960

Figure Lengend Snippet: ROS mediates the inflammatory response of periodontal membrane fibroblasts under hypoxia. (a) ROS in HPDLCs after 24 h treatment with or without 2 mM NAC in the normal group and CoCl 2 -induced hypoxia environment. (b) Degree of aggregation of immunofluorescence staining (IF) in periodontal membrane fibroblasts after 24 h treatment with or without 2 mM NAC in the normal group and CoCl 2 -induced hypoxia environment. (c) RT-PCR analysis of TXNIP, NLRP3, ASC, caspase-1, and IL-1 β in periodontal membrane fibroblasts after 24 h treatment with or without 2 mM NAC in the normal group and CoCl 2 -induced hypoxia environment. (d) Western blotting analysis of TXNIP, NLRP3, ASC, caspase-1, and IL-1 β in periodontal fibroblasts treated with or without 2 mM NAC for 24 h in the normal group and CoCl 2 -induced hypoxia environment. The above data are presented as the mean ± SEM, ∗ p < 0.05.

Article Snippet: Membranes were blocked with 5% skimmed milk in TBST for 1 h at room temperature and then incubated with the following primary antibodies overnight at 4°C: TXNIP (Rabbit IgG, Boster, China), NLRP3 (Rabbit IgG, Boster, China), ASC (Rabbit IgG, Immunoway, China), and caspase-1 (Rabbit IgG, Immunoway, China) at 1 : 1000.

Techniques: Membrane, Immunofluorescence, Staining, Reverse Transcription Polymerase Chain Reaction, Western Blot