Fig 1: Intestinal permeability led to leakage of LPS intothe systemic circulation and stimulated the immune response and neuro-inflammation, which further increase the BBB permeability and deregulation in serum levels of S100B; also neuro-inflammation was able to alter the BDNF levels, which may have caused disorders in follicular growth. By interfering with LPS leakage and antioxidant properties, thylakoids may have impaired this series of disorders in PCOS patientsAbbreviations: BBB: blood-brain barrier; BDNF: brain-derived neurotrophic factor; LPS: lipopolysaccharides; NF-κB: nuclear factor kappa B; ROS: reactive oxygen species; S100B: S100 calcium-binding protein B
Fig 2: ELISA detection of S100B levels. (A) The SLE patients with neurologic disorder (125.08 ± 20.34 pg/mL, n=71) showed higher serum S100B levels than non-neurologic disorder patients (112.30 ± 27.98 pg/mL, n=71) and controls (97.16 ± 20.34 pg/mL, n=71), respectively [both p < 0.05]. (ND-neurologic disorder). (B) The SLE patients with neurologic disorder carrying the rs1051169 CC genotype (140.29 ± 28.17 pg/mL, n=24) showed significantly higher serum S100B levels than whose with GC (122.47 ± 24.11 pg/mL, n=35) and GG genotype (102.24 ± 18.26 pg/mL, n=12), respectively (both p < 0.05).
Fig 3: Intracolonic administration of HIV-1 Tat induced glial activation in the (a) thoracic and (b) cervical spinal cord and (c) frontal cortex at day 12, 14 and 21 after diarrhea induction, respectively. (a–c) Immunofluorescence analysis showed that iNOS (green) and S100B (red) co-expression was increased in the spinal cord and frontal of HIV-1 Tat treated rats. (d–f) Quantitative analysis showed that HIV-1 Tat-induced upregulation of iNOS (filled bars) and S100B (open bars) was significantly inhibited by lidocaine treatment. Results are expressed as mean ± SEM; ***p < 0.001 vs all other groups; °°°p < 0.001 vs HIV-1 Tat group. Scale bars: 100 μm; n = 6 for each group.
Fig 4: Pearson correlations between MMSE scores and relevant factors in COPD groups. ▼ = serum S100B concentrations; ▲ = PaO2; ■ = FEV1% predicted. A = mild-to-moderate COPD group: S100B (r = −0.40, P < 0.01); B = severe COPD group: S100B (r = −0.31, P < 0.01); C = mild-to-moderate COPD group: PaO2 (r = 0.59, P < 0.01); D = severe COPD group: PaO2 (r = 0.46, P < 0.01); FEV1 (r = 0.35, P < 0.05).
Fig 5: (a,b) EMSA analysis showing that intracolonic administration of HIV-1 Tat (100 ng/ml) induced a marked increase of NF-kappaB expression in EGCs nuclear extracts versus vehicle group. The administration of lidocaine significantly reduced HIV-1 Tat-induced NF-kappaB activation, whereas bisacodyl failed to induce any significant effect on NF-kappaB activation. (a) The panel shows representative NF-kappaB activation complex bands and (b) their densitometric quantification (OD = optical density in mm2). (c,d) HIV-1 Tat treatment caused a marked increase of GFAP, S100B, TLR-4 and iNOS protein expression in submucosal plexus lysates, as compared to vehicle group and this effect was significantly inhibited by lidocaine; to note that bisacodyl also failed to induce any significant effect. (c) The panel shows representative immunoreactive bands of analyzed proteins and (d) their respective levels expressed as fold change. (e,f) In the medium of submucosal plexi lysates obtained from HIV-1 Tat treated rats a significant increase of NO2 − and S100B was observed in comparison with vehicle group and such effect was counteracted by lidocaine; again, bisacodyl had no effect on treated animals. Results are expressed as mean ± SEM; ***p < 0.001 vs all other groups; °°°p < 0.001 vs HIV-1 Tat group; n = 6 for each group.
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