Journal: Molecular Pain

Article Title: Targeting Vascular endothelial growth factor A with soluble vascular endothelial growth factor receptor 1 ameliorates nerve injury-induced neuropathic pain

doi: 10.1177/17448069221094528

Figure Lengend Snippet: rpVEGF induces mechanical and thermal hyperalgesia. (A). Effect of Vascular endothelial growth factor A (rpVEGFA) on the paw withdrawal mechanical threshold (PWMT). After 1 ng, 10 ng and 100 ng rpVEGFA i.t. injection, the PWMT was significantly decreased when compared to control mice; (B). Effect of rpVEGFA on the paw withdrawal thermal latency (PWTL). Compared with the control group, the PWTL was dramatically reduced after 1 ng, 10 ng and 100 ng rpVEGFA i.t. injection. The results were analyzed by One-way analysis of variance (ANOVA) and by multiple comparisons. ( n = 6). * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: The membrane was blocked with 5% bovine serum albumin (BSA) for 1 h at room temperature and incubated overnight at 4°C with primary antibodies against VEGFA, IL-6, TNF-α, IL-1β (1:2000, rabbit; Proteintech), VEGFR2, AKT, p-p38 (1:2000, rabbit; Cell Signaling), p-AKT (1:2000, rabbit, Affinity), and transient receptor potential vanilloid type 1 (TRPV1, 1:2000, rabbit, Alomone Labs).

Techniques: Injection, Control

Journal: Molecular Pain

Article Title: Targeting Vascular endothelial growth factor A with soluble vascular endothelial growth factor receptor 1 ameliorates nerve injury-induced neuropathic pain

doi: 10.1177/17448069221094528

Figure Lengend Snippet: Immunofluorescence analyses the expression of VEGFA, p-AKT, and TRPV1 in the spinal cord. (a–d). VEGFA (green), p-AKT (red), and TRPV1(red) are mainly expressed in the superficial dorsal horn region (laminae I-II) of the spinal cord. The expression of VEGFA, p-AKT, and TRPV1 was robustly increased in SNI mice, but sFlt1 inhibited this increase (green, b and d). The average optical densities (AODs) in the images were quantified by ImageJ. The data are shown as the mean ± SEM ( n = 3). The results were analyzed by One-way ANOVA and by multiple comparisons. ⁎ p < .05, ⁎⁎ p < .01, and ⁎⁎⁎ p < .001. TRPV1, transient receptor potential vanilloid type 1.

Article Snippet: The membrane was blocked with 5% bovine serum albumin (BSA) for 1 h at room temperature and incubated overnight at 4°C with primary antibodies against VEGFA, IL-6, TNF-α, IL-1β (1:2000, rabbit; Proteintech), VEGFR2, AKT, p-p38 (1:2000, rabbit; Cell Signaling), p-AKT (1:2000, rabbit, Affinity), and transient receptor potential vanilloid type 1 (TRPV1, 1:2000, rabbit, Alomone Labs).

Techniques: Immunofluorescence, Expressing

Journal: BMC Neuroscience

Article Title: Histone deacetylase inhibitor SAHA attenuates post-seizure hippocampal microglia TLR4/MYD88 signaling and inhibits TLR4 gene expression via histone acetylation

doi: 10.1186/s12868-016-0264-9

Figure Lengend Snippet: Nucleotide sequences of primers for real time quantitative polymerase chain reaction

Article Snippet: The membranes were soaked in 5 % skimmed milk as blocking buffer for 2 h and then incubated with appropriate primary antibodies including mouse anti-TLR4 antibody (1:1000; Abcam), rabbit anti-MYD88 antibody (1:1000; Cell Signaling, Beverly, MA, USA), rabbit anti-NF-kB P65 antibody (1:2000; Proteintech), rabbit anti-IL-1β antibody (1:500, Proteintech) and mouse anti-β-actin (1:2000; Abcam), respectively, at 4 °C overnight.

Techniques:

Journal: BMC Neuroscience

Article Title: Histone deacetylase inhibitor SAHA attenuates post-seizure hippocampal microglia TLR4/MYD88 signaling and inhibits TLR4 gene expression via histone acetylation

doi: 10.1186/s12868-016-0264-9

Figure Lengend Snippet: SAHA attenuated KA-induced seizures behavior in rats. The rats were pretreated with SAHA (10 or 50 mg/kg, i.p.) 30 min before KA (15 mg/kg, i.p.) injection. Seizure latency was measured during 1–4 h after KA administration. Data are expressed as mean ± SD. ***P < 0.001; **P < 0.01 or *P < 0.05 versus KA-treated group

Article Snippet: The membranes were soaked in 5 % skimmed milk as blocking buffer for 2 h and then incubated with appropriate primary antibodies including mouse anti-TLR4 antibody (1:1000; Abcam), rabbit anti-MYD88 antibody (1:1000; Cell Signaling, Beverly, MA, USA), rabbit anti-NF-kB P65 antibody (1:2000; Proteintech), rabbit anti-IL-1β antibody (1:500, Proteintech) and mouse anti-β-actin (1:2000; Abcam), respectively, at 4 °C overnight.

Techniques: Injection

Journal: BMC Neuroscience

Article Title: Histone deacetylase inhibitor SAHA attenuates post-seizure hippocampal microglia TLR4/MYD88 signaling and inhibits TLR4 gene expression via histone acetylation

doi: 10.1186/s12868-016-0264-9

Figure Lengend Snippet: SAHA inhibited TLR4 signal pathway in KA-induced seizures. The protein expression of TLR4, MYD88, NF-κB P65 and IL-1β were examined by immunoblots at 2, 6 h, 1 d and 2 d after KA injection in hippocampus CA1 region. Specific bands were quantified by densitometry and data were expressed as mean ± SD (n = 3); # P < 0.01 versus control group; *P < 0.01 versus KA-treated group

Article Snippet: The membranes were soaked in 5 % skimmed milk as blocking buffer for 2 h and then incubated with appropriate primary antibodies including mouse anti-TLR4 antibody (1:1000; Abcam), rabbit anti-MYD88 antibody (1:1000; Cell Signaling, Beverly, MA, USA), rabbit anti-NF-kB P65 antibody (1:2000; Proteintech), rabbit anti-IL-1β antibody (1:500, Proteintech) and mouse anti-β-actin (1:2000; Abcam), respectively, at 4 °C overnight.

Techniques: Expressing, Western Blot, Injection, Control

Journal: BMC Neuroscience

Article Title: Histone deacetylase inhibitor SAHA attenuates post-seizure hippocampal microglia TLR4/MYD88 signaling and inhibits TLR4 gene expression via histone acetylation

doi: 10.1186/s12868-016-0264-9

Figure Lengend Snippet: SAHA attenuated KA-induced mRNA expression of TLR4, MYD88, NF-κB and IL-1β in hippocampus. In hippocampus CA1 region, mRNA expression of TLR4, MYD88, NF-κB and IL-1β were measured with real-time Quantitative PCR at 2, 6 h, 1 d and 2 d after KA injection. Relative quantification data were expressed as mean ± SD (n = 3). # P < 0.01 versus control group; *P < 0.01 versus KA-treated group

Article Snippet: The membranes were soaked in 5 % skimmed milk as blocking buffer for 2 h and then incubated with appropriate primary antibodies including mouse anti-TLR4 antibody (1:1000; Abcam), rabbit anti-MYD88 antibody (1:1000; Cell Signaling, Beverly, MA, USA), rabbit anti-NF-kB P65 antibody (1:2000; Proteintech), rabbit anti-IL-1β antibody (1:500, Proteintech) and mouse anti-β-actin (1:2000; Abcam), respectively, at 4 °C overnight.

Techniques: Expressing, Real-time Polymerase Chain Reaction, Injection, Quantitative Proteomics, Control

Journal: Frontiers in Bioengineering and Biotechnology

Article Title: Polyvinylpyrrolidone-Modified Taxifolin Liposomes Promote Liver Repair by Modulating Autophagy to Inhibit Activation of the TLR4/NF-κB Signaling Pathway

doi: 10.3389/fbioe.2022.860515

Figure Lengend Snippet: Inflammatory factors in mice with ALI induced by LPS/D-GalN. (A) Protein levels of iNOS, IL-1β, TNF-α, and β-actin analyzed by Western blotting. (B–D) Relative band intensity analyzed by ImageJ Analysis System, and β-actin was used as a control for equal loading. As compared with the control group, # p < 0.05. As compared with the model group, * p < 0.05. The data are presented as the mean ± SD ( n = 3).

Article Snippet: Rabbit primary polyclonal antibodies to Toll-like receptor 4 (TLR4), myeloid differentiation factor88 (MyD88), nuclear factor-kappa B (NF-κB, P65), sequestosome-1 (P62), light chain 3 (LC3), mouse Interleukin-1β (IL-1β), inducible nitric oxide synthase (iNOS), tumor necrosis factor α (TNF-α), β-actin, Autophagy related 7 (ATG7), Autophagy related 5 (ATG5), inhibitor kappa B alpha (IκBα), phospho-inhibitor kappa B alpha (p-IκBα), goat anti-rabbit IgG horseradish peroxidase (HRP)-conjugated secondary antibody, and goat anti-mouse IgG-HRP-conjugated secondary antibody were bought from Proteintech (Wuhan, China).

Techniques: Western Blot, Control