Journal: Biochemistry and biophysics reports

Article Title: NanoLuciferase technology-based detection of TMPRSS2 as attempt to develop anti-coronavirus agents.

doi: 10.1016/j.bbrep.2024.101783

Figure Lengend Snippet: Fig. 1. Normalized TMPRSS2-HiBiT signal under treatment of compounds from (A) diversified building block library, (B) bioactive compound library, or (C) human endogenous metabolite library, at concentration of 10 μM and adjusted to corresponding ATP-Glo signal.

Article Snippet: Diversified building block compound library, bioactive compound library and endogenous metabolite compound library were from TargetMol.

Techniques: Blocking Assay, Drug discovery, Concentration Assay

Journal: Frontiers in Neurology

Article Title: Exosomal circ_0093708 as a potential ferroptosis biomarker in cerebral ischemia–reperfusion injury

doi: 10.3389/fneur.2025.1633393

Figure Lengend Snippet: Mining of key genes for ferroptosis and verification in external databases. (A) The 5-set Venn diagram showing the comprehensive strategy among suppressor ferroptosis-associated genes (green circle), unclassified ferroptosis-associated genes (orange circle), marker ferroptosis-associated genes (blue circle), driver ferroptosis-associated genes (pink circle), and differentially expressed genes (DEGs) (purple circle). (B) ROC analysis for DUSP1 in the discovery dataset. (C) ROC analysis for PTGS2 in the discovery dataset. (D) ROC analysis for DUSP1 in the validation dataset. (E) ROC analysis for PTGS2 in the validation dataset. ROC, receiver operating characteristic.

Article Snippet: We chose CIL56 (T4309, TargetMol, America) to construct the ferroptosis model under the condition of 0.7 μM for 24 h. (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) is a commonly used inhibitor of MKP-1.

Techniques: Marker, Biomarker Discovery

Journal: Frontiers in Neurology

Article Title: Exosomal circ_0093708 as a potential ferroptosis biomarker in cerebral ischemia–reperfusion injury

doi: 10.3389/fneur.2025.1633393

Figure Lengend Snippet: Inhibition of DUSP1 exacerbates ferroptosis in PC12 cells. (A) Cell viability after CIL56 treatment. (B) Intracellular MDA levels. (C) Effect of BCI on DUSP1 inhibition in the ferroptosis model. (D) Intracellular ROS levels (scale bar: 20 μm). (E) Protein expression of DUSP1, GPX4, and TFRC. (F) Quantification of GPX4 levels. (G) Quantification of TFRC levels. Data were analyzed by one-way ANOVA with Tukey’s post hoc test and presented as mean ± SD. Con, control.

Article Snippet: We chose CIL56 (T4309, TargetMol, America) to construct the ferroptosis model under the condition of 0.7 μM for 24 h. (E)-2-benzylidene-3-(cyclohexylamino)-2,3-dihydro-1H-inden-1-one (BCI) is a commonly used inhibitor of MKP-1.

Techniques: Inhibition, Expressing, Control

Journal: Neural Regeneration Research

Article Title: Hypoxia-preconditioned bone marrow–derived mesenchymal stem cells protect neurons from cardiac arrest–induced pyroptosis

doi: 10.4103/NRR.NRR-D-23-01922

Figure Lengend Snippet: PFKL mediates the neuroprotective and antioxidant effects of HP-BMSCs in CPR rats. (A) Neurological deficit scores (NDS) in four group (CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). The black line represents the NDS levels in the sham group. (B) Serum S100B levels after treatment as indicated ( n = 8). (C) Nissl staining of rat brains after CPR in different group (sham, CPR + PBS, CPR + HP-BMSCs, CPR + si NC HP-BMSCs, CPR + si-PFKL HP-BMSCs, n = 8). After 24 hours of resuscitation, the number of Nissl bodies in the rat cortex significantly decreased, and transplantation of HP-BMSCs could alleviate the reduction of Nissl bodies. However, this effect of HP-BMSCs was reversed after knocking down PFKL. Scale bars: 100 μm (upper) or 50 μm (lower). (D) The AOD of cortical neurons by Nissl staining. (E, F) Representative immunohistochemical staining of 4-HNE (E) and 8-OHdG (F) in cortex following ROSC. After transplantation of HP-BMSCs, the expression of 4-HNE and 8-OHdG in the cortex of CA/CPR rats significantly decreased, whereas this effect was attenuated after knocking down PFKL. The selected areas (black frame) were displayed at a higher magnification level. Scale bars: 70 μm (upper) or 50 μm (lower). (G, H) Percentage of 4-HNE-positive cells (G) and 8-OHdG-positive cells (H) in immunohistochemical images ( n = 8). (I–K) Histograms show the expression of SOD (I), GSH-Px (J) and MDA (K). n = 6 rats per group. (L) Representative images show iNOS (green, Alexa Fluor 488) immunostaining with NeuN (red, CY3) and DAPI (blue) in the cotex ( n = 8). The white boxed areas are shown magnified. HP-BMSCs significantly reduced the expression of iNOS in the neurons of CA-induced rats, while knocking down the expression of PFKL in HP-BMSCs did not lead to significant changes in the expression of iNOS. Scale bars: 50 μm (lower) or 1000 μm (upper). (M) Percentage of iNOS-positive neurons in immunofluorescence images. (N) ROS generation in cortex post-resuscitation was assayed by ROS assay kit. Compared with the si-NC HP-BMSCs group, the reduction effect of si-PFKL HP-BMSCs on post-resuscitation cortical ROS is significantly weakened. The fluorescence was detected by the fluorescence microplate reader ( n = 3). Scale bars: 100 μm. (O) The fluorescent intensity of ROS shown in N. Results expressed as median and interquartile range (A and D) or means ± SD (G–K, M and O). * P < 0.05, vs . sham group; # P < 0.05, vs . CPR + PBS group; & P < 0.05, vs . CPR + si-NC-BMSCs group (Kruskal–Wallis test followed by Dunn’s multiple comparisons test in A and D; one-way analysis of variance followed by Tukey’s multiple comparisons test in G–K, M and O). 4-HNE: 4-Hydroxynonenal; 8-OHdG: 8-hydroxy-2′-deoxyguanosine; AOD: average optical density; CPR: cardiopulmonary resuscitation; HP-BMSCs: hypoxia preconditioned bone marrow mesenchymal stem cells; iNOS: inducible nitric oxide synthase; MDA: malondialdehyde; PBS: phosphate-buffered saline; PFKL: liver isoform of phosphofructokinase; ROI: region of interest; ROS: reactive oxygen species; ROSC: return of spontaneous circulation; SOD: superoxide dismutase.

Article Snippet: For the second experiment, the cells were divided into five groups that were left untreated or treated with siRNAs, left untreated or treated with 10 μM mitochondria-targeted antioxidant (Mito-TEMPO, TargetMol, Shanghai.

Techniques: Staining, Transplantation Assay, Immunohistochemical staining, Expressing, Immunostaining, Immunofluorescence, ROS Assay, Fluorescence, Analysis, Saline, Immunohistochemistry, Knockdown