HY-151573 Search Results


m indanyloxyacetic acid 94  (MedChemExpress)
97
MedChemExpress m indanyloxyacetic acid 94
M Indanyloxyacetic Acid 94, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/m indanyloxyacetic acid 94/product/MedChemExpress
Average 97 stars, based on 1 article reviews
m indanyloxyacetic acid 94 - by Bioz Stars, 2026-02
97/100 stars
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stat3 inhibitor  (MedChemExpress)
94
MedChemExpress stat3 inhibitor
IL-22 negatively regulates BBB integrity by activating <t>STAT3.</t> (A) Western blot analysis of STAT3 phosphorylation in hBMEC in response to multiple doses of IL-22 (0, 1, 5, 10, 20, and 100 ng/mL). β-Actin was used as the loading control. Densitometry was performed to analyze differences among the samples. *** p < 0.001. (B) ECIS system monitoring TEER changes of the IL-22-treated hBMEC with or without STAT3 specific inhibitor S3I-201 administration. Data were collected and presented as mean ± SD from three independently replicated wells at each time point. (C) Effects of the S3I-201 (50 μM) treatment on IL-22-induced (10 ng/mL) downregulation of ZO-1, Occludin, and Claudin-5 in hBMEC. β-Actin was used as the loading control. Densitometry was performed to analyze differences among the samples. ** p < 0.01, *** p < 0.001. (D) Distribution of TJPs in IL-22-treated hBMEC with or without S3I-201 (50 μM) administration, as determined by immunofluorescence analysis. ZO-1, Occludin, and Claudin-5 were stained in red. The cell nucleus was stained in blue with DAPI. Scale bar, 10 μm.
Stat3 Inhibitor, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/stat3 inhibitor/product/MedChemExpress
Average 94 stars, based on 1 article reviews
stat3 inhibitor - by Bioz Stars, 2026-02
94/100 stars
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Image Search Results


IL-22 negatively regulates BBB integrity by activating STAT3. (A) Western blot analysis of STAT3 phosphorylation in hBMEC in response to multiple doses of IL-22 (0, 1, 5, 10, 20, and 100 ng/mL). β-Actin was used as the loading control. Densitometry was performed to analyze differences among the samples. *** p < 0.001. (B) ECIS system monitoring TEER changes of the IL-22-treated hBMEC with or without STAT3 specific inhibitor S3I-201 administration. Data were collected and presented as mean ± SD from three independently replicated wells at each time point. (C) Effects of the S3I-201 (50 μM) treatment on IL-22-induced (10 ng/mL) downregulation of ZO-1, Occludin, and Claudin-5 in hBMEC. β-Actin was used as the loading control. Densitometry was performed to analyze differences among the samples. ** p < 0.01, *** p < 0.001. (D) Distribution of TJPs in IL-22-treated hBMEC with or without S3I-201 (50 μM) administration, as determined by immunofluorescence analysis. ZO-1, Occludin, and Claudin-5 were stained in red. The cell nucleus was stained in blue with DAPI. Scale bar, 10 μm.

Journal: ACS Infectious Diseases

Article Title: Interleukin-22 Contributes to Blood–Brain Barrier Disruption via STAT3/VEGFA Activation in Escherichia coli Meningitis

doi: 10.1021/acsinfecdis.3c00668

Figure Lengend Snippet: IL-22 negatively regulates BBB integrity by activating STAT3. (A) Western blot analysis of STAT3 phosphorylation in hBMEC in response to multiple doses of IL-22 (0, 1, 5, 10, 20, and 100 ng/mL). β-Actin was used as the loading control. Densitometry was performed to analyze differences among the samples. *** p < 0.001. (B) ECIS system monitoring TEER changes of the IL-22-treated hBMEC with or without STAT3 specific inhibitor S3I-201 administration. Data were collected and presented as mean ± SD from three independently replicated wells at each time point. (C) Effects of the S3I-201 (50 μM) treatment on IL-22-induced (10 ng/mL) downregulation of ZO-1, Occludin, and Claudin-5 in hBMEC. β-Actin was used as the loading control. Densitometry was performed to analyze differences among the samples. ** p < 0.01, *** p < 0.001. (D) Distribution of TJPs in IL-22-treated hBMEC with or without S3I-201 (50 μM) administration, as determined by immunofluorescence analysis. ZO-1, Occludin, and Claudin-5 were stained in red. The cell nucleus was stained in blue with DAPI. Scale bar, 10 μm.

Article Snippet: For inhibitor treatment, hBMEC were pretreated with STAT3 inhibitor 50 μM S3I-201 (HY-15146, MCE, Monmouth Junction, NJ) and dimethyl sulfoxide (DMSO) 9 h before 10 ng/mL IL-22 administration.

Techniques: Western Blot, Phospho-proteomics, Control, Immunofluorescence, Staining

Effects of the IL-22/STAT3 axis on VEGFA expression. (A) Western blot analysis of VEGFA expression in hBMEC in response to multiple doses of IL-22 (0, 1, 2, 5, and 10 ng/mL). β-actin was used as the loading control. Densitometry was performed to analyze differences among the samples. ** p < 0.01. (B) ELISA analysis of VEGFA in serum and brain lysates from challenged WT and IL-22 –/– mice. Data were collected and presented as mean ± SD * p < 0.05, *** p < 0.001. (C) ChIP-PCR validation of the STAT3 binding to the VEGFA promoter in hBMEC treated with 10 ng/mL IL-22. The nuclear extracts were immunoprecipitated with anti-p-STAT3 antibody or normal IgG and a ChIP assay was performed. The PCR primers were amplified in the −913 to −783 region of the VEGF promoter. Input refers to the same dose of nuclear extract administered prior to immunoprecipitation. (D) Western blot analysis of the effect of S3I-201 (50 μM) treatment on the IL-22-increased (10 ng/mL) VEGFA levels in hBMEC. β-actin was used as the loading control. Densitometry was performed to analyze differences among the samples. ** p < 0.01.

Journal: ACS Infectious Diseases

Article Title: Interleukin-22 Contributes to Blood–Brain Barrier Disruption via STAT3/VEGFA Activation in Escherichia coli Meningitis

doi: 10.1021/acsinfecdis.3c00668

Figure Lengend Snippet: Effects of the IL-22/STAT3 axis on VEGFA expression. (A) Western blot analysis of VEGFA expression in hBMEC in response to multiple doses of IL-22 (0, 1, 2, 5, and 10 ng/mL). β-actin was used as the loading control. Densitometry was performed to analyze differences among the samples. ** p < 0.01. (B) ELISA analysis of VEGFA in serum and brain lysates from challenged WT and IL-22 –/– mice. Data were collected and presented as mean ± SD * p < 0.05, *** p < 0.001. (C) ChIP-PCR validation of the STAT3 binding to the VEGFA promoter in hBMEC treated with 10 ng/mL IL-22. The nuclear extracts were immunoprecipitated with anti-p-STAT3 antibody or normal IgG and a ChIP assay was performed. The PCR primers were amplified in the −913 to −783 region of the VEGF promoter. Input refers to the same dose of nuclear extract administered prior to immunoprecipitation. (D) Western blot analysis of the effect of S3I-201 (50 μM) treatment on the IL-22-increased (10 ng/mL) VEGFA levels in hBMEC. β-actin was used as the loading control. Densitometry was performed to analyze differences among the samples. ** p < 0.01.

Article Snippet: For inhibitor treatment, hBMEC were pretreated with STAT3 inhibitor 50 μM S3I-201 (HY-15146, MCE, Monmouth Junction, NJ) and dimethyl sulfoxide (DMSO) 9 h before 10 ng/mL IL-22 administration.

Techniques: Expressing, Western Blot, Control, Enzyme-linked Immunosorbent Assay, Biomarker Discovery, Binding Assay, Immunoprecipitation, Amplification