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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: The overexpression of TDP-43 in astrocytes causes neurodegeneration via a PTP1B-mediated inflammatory response

Fig. 2

PTP1B inhibition suppresses TDP-43-induced inflammation via the NF-κB pathway. ac TDP-43-Gfp-transfected astrocytes were treated with PTP1B inhibitor (PTP1Bi, 5 μM) for 24 h and then were analysed by immunoblotting. a Immunoblot analysis of Gfp- or TDP-43-Gfp-transfected cells was performed to detect the protein expression of phosphorylated NF-κB (Ser536) and total NF-κB after PTP1B inhibitor (PTP1Bi, 5 μM) treatment for 24 h. Tubulin was used for normalization. Data are presented as the mean ± SD. **p < 0.005; ***p < 0.001 (one-way ANOVA). b Expression of Gfp- or TDP-43-Gfp in cells was confirmed by immunoblotting using an anti-TDP-43 or anti-GFP antibody. Tubulin was used for normalization. c Cells were fractionated into nuclear and cytoplasmic extracts. Immunoblot analysis was performed for NF-κB protein in the nuclear and cytoplasmic fractions. Lamin A/C (nuclear fraction) and tubulin (cytoplasmic fraction) were used for normalization. Data are presented as the mean ± SD. *p < 0.05; N.S. not significant (one-way ANOVA). df Gfp- or TDP-43-Gfp-transfected astrocytes were treated with a PTP1B inhibitor (PTP1Bi, 5 μM) for 24 h, and then the ACMs were harvested. ELISAs were conducted for secreted cytokines (IL-1β, IL-6 and TNF-α) in the GFP ACM, TDP-43 ACM and TDP-43 + PTP1Bi ACM groups. Data are presented as the mean ± SD. *p < 0.05; **p < 0.005; and ***p < 0.001 (one-way ANOVA). g A CCK-8 assays were performed to assess the viability of primary astrocytes treated with the PTP1B inhibitor (PTP1Bi, 5 μM, 10 μM or 20 μM) for 24 h. Data are presented as the mean ± SD

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