Journal: International Journal of Medical Sciences

Article Title: Hyperbaric oxygen protects against periodontal bone loss by modulating inflammation and bone remodeling via RANKL/OPG expression in ligature-induced periodontitis

doi: 10.7150/ijms.122857

Figure Lengend Snippet: HBOT reduces gingival cytokine and chemokine expression in ligature-induced periodontitis. (A) Representative cytokine array blots showing expression profiles of 10 key inflammatory mediators (red boxes) in gingival tissues collected at day 14 and day 28 from Sham, PD+RECOV (natural recovery), PD (periodontitis only), PD+EHBOT (early HBOT), and PD+LHBOT (late HBOT) groups. The targeted proteins included: 1. CINC-1 (CXCL1), 2. CINC-2α/β (CXCL3), 3. sICAM-1, 4. IL-1α, 5. IL-1β, 6. IL-1 receptor antagonist (IL-1ra), 7. LIX (CXCL5), 8. L-selectin (CD62L), 9. Thymus chemokine (CCL25), and 10. TIMP-1. (B) Quantitative analysis of cytokine and chemokine expression at day 14. Periodontitis induced marked increases in several pro-inflammatory cytokines and chemokines. Early HBOT significantly suppressed most inflammatory mediators compared to the PD and PD+RECOV groups. (C) Quantitative analysis at day 28. PD-induced cytokine elevation persisted, while both early and late HBOT treatments effectively reduced IL-1α, IL-1β, IL-1ra, sICAM-1, CINC-1, CINC-2α/β, LIX, and thymus chemokine levels. Notably, early HBOT more effectively reduced thymus chemokine expression than natural recovery. Data are presented as mean ± SD. n = 6 per group. Panel 2A shows a cytokine dot-array membrane (R&D Systems ARY008) from a single, intact exposure; the published panel was border-cropped only to remove blank margins (global linear contrast, no compositing). See Supplementary for the full, uncropped membrane and original X-film/RAW.

Article Snippet: Protein extracts (200 μg per sample) were applied to Rat Cytokine Antibody Arrays (ARY008, R&D Systems, Inc., USA), which detect a panel of 34 inflammatory cytokines, chemokines, and adhesion molecules.

Techniques: Expressing, Membrane

Journal: JCI Insight

Article Title: Innate immune activation and mitochondrial ROS induce acute and persistent cardiac conduction system dysfunction after COVID-19

doi: 10.1172/jci.insight.193164

Figure Lengend Snippet: ( A ) Schematic of molecular mechanisms of COVID-19 and dsRNA induced IFN response. Ruxolitinib suppresses IFN-stimulated response and mitoTEMPO suppresses mitochondrial damage and oxidative stress. (Created with BioRender.com.) ( B and C ) Inhibition of JAK/STAT signaling with ruxolitinib (Rux) (1 μM) significantly suppressed PIC-mediated induction of the interferon response signaling proteins STAT1, p-STAT1, IRF9, and MX1 in hiPSC-CM monolayers. MitoTEMPO (MT) (1 μM) does not significantly suppress the IFN response. Bar graphs show relative band intensity normalized to total protein loading (1-way ANOVA with Tukey’s multiple-comparison test). Lysates were from 3–5 different hiPSC-CM samples. ( C ) Inhibition of JAK/STAT signaling in hiPSC-derived engineered heart tissues (EHTs) with ruxolitinib, but not mitoTEMPO (MT), decreased the interferon response of signaling proteins STAT1, pSTAT1, IRF9, and MX1. Lysates loaded for the Western blot in C were from 3 different EHTs. ( D ) Cytokine secretion into the media induced by PIC, measured using a human Proteome Profiler array (inset shows exemplar blots), was greatly suppressed by Rux treatment in hiPSC-CM.

Article Snippet: Using a human cytokine antibody array (Proteome Profiler, R&D Systems), we found that PIC induced the secretion of a plethora of cytokines into the media from hiPSC-CM, including a >2-fold increase in 36 of the 105 cytokines assayed ( and ).

Techniques: Inhibition, Comparison, Derivative Assay, Western Blot