human clec7a protein  (R&D Systems)

Journal: bioRxiv

Article Title: Dynamic Reprogramming of Fungal Cell Walls Underlies Germination and Immune Exposure in Zygomycetous Fungal Pathogens

doi: 10.64898/2026.05.12.724644

Figure Lengend Snippet: ( A ) TEM images of the dormant conidia reveal a multilayered cell wall architecture, including an electron-dense outer layer and inner polysaccharide-rich regions. ( B ) At high magnification, osmium-fixed, epoxy-embedded samples (left) preserve structural integrity, whereas LR White–embedded samples prepared without OsO 4 (right) enhance contrast in the outer wall. Sub-labels denote (i) outer electron-dense region, (ii) granular region, and (iii) electron-lucent inner layer. Without OsO 4 , the outer layer appears as a thin electron-lucent band consistent with melanin, with the remaining regions largely electron-lucent. ( C ) Rigid molecules in the dormant conidial cell walls were detected by 2D 13 C- 13 C CORD spectra, showing signals from β-1,3-glucan (B), chitin (Ch), and chitosan (Cs). Superscripts indicate different structural forms of each polysaccharide, and the numbers denote carbon positions. For example, Cs a 1-2 represents the correlation between carbons 1 and 2 in type-a chitosan. ( D ) Structural representations of carbohydrates. Yellow bars indicate whether each molecule is detected in the rigid phase, the mobile phase, or in both. NMR abbreviations are given. Key carbon sites are numbered. ( E ) Composition of rigid carbohydrates in dormant conidia based on intensity analysis of the 2D CORD spectrum. ( F ) Overlay of 2D CORD spectra of dormant conidia (blue) and 3-day-old mycelia (orange). ( G ) Cytochemical labeling of dormant conidia shows gold-specific staining for β-1,3-glucan with Fc-Dectin-1, chitin (with Wheat germ agglutinin lectin (WGA-lectin), and anti-chitosan rabbit antiserum. Black dots represent electron-dense gold particles indicating probe binding. Scale bars: 500 nm. ( H ) Mobile molecules in dormant conidia detected by the 2D 13 C-DP refocused J-INADEQUATE spectrum. In addition to β-1,3-glucan and two forms of chitosan, signals are detected for Fuc (F), Gal, α-1,2-Man (Mn , ), and α-1,6-Man (Mn , ). ( I ) Cytochemical binding of Concanavalin-A lectin (ConA) to dormant conidial cell walls confirms the presence of mannans and/or glycoproteins. Zoomed-in view of 2D 13 C-DP J-INADEQUATE spectrum was presented for ( J ) C5-C6 correlations of polymeric fucoses and ( K ) glucuronic acid (GlcA). Polymeric fucoses show five forms (a,b, c, d, i) as traced by dashed lines in dormant conidia (blue) while type-e is present only in mycelia (orange).

Article Snippet: Grids were washed with endotoxin-free water and incubated for 1 h with 100 μg mL -1 recombinant human Fc-Dectin-1 (Fc-hDectin-1a, InvivoGen).

Techniques: Labeling, Staining, Binding Assay

Journal: bioRxiv

Article Title: Dynamic Reprogramming of Fungal Cell Walls Underlies Germination and Immune Exposure in Zygomycetous Fungal Pathogens

doi: 10.64898/2026.05.12.724644

Figure Lengend Snippet: ( A ) TEM images of germinating conidia showing swollen conidia undergoing isotropic expansion at 1 h (left), swollen conidia with rupture of the outer cell wall enabling emergence of a polarized germ tube (middle), and elongated germ tubes (right). Magenta arrows indicate changes in the outer wall, while yellow arrows highlight the thinner inner layer that extends and contributes to germ tube wall formation. ( B ) Violin plot showing the reduction in cell wall thickness from dormant conidia (DC) to swollen (SW) and germ tube (GT) stages (n=120 per group). ( C ) 1D 13 C CP spectra detecting only neosynthesized polysaccharides in germinating 12 C-conidia grown in 13 C-labeled media (inset). Spectra were collected at different time points of 1 h (black), 2.5 h (green), and 5 h (magenta). Dashed lines highlight the signature peaks of chitin, β-1,3-glucan, and chitosan. ( D ) Molar composition of rigid neo-synthesized polysaccharides (%) in the 1-5 h culture. Compositional percentages are calculated by deconvoluting 1D 13 C CP spectra. ( E ) 2D 13 C- 13 C CORD spectra of the 5 h culture, with blue circles indicating the absence of β-1,3-glucan signals. ( F ) Cytochemical labeling of gold-specific staining for β-1,3-glucan (with Fc-Dectin-1, top), chitin (with WGA-lectin, middle), and anti-chitosan rabbit antiserum (bottom). Scale bars: 500 nm. Electron-dense gold particles (black dots) mark probe binding. The newly formed thin cell wall of germ tube (orange arrowheads) is labeled by WGA and anti-chitosan. Dectin labeling is only positive in the cell wall of the original resting conidium cell wall. Magenta arrows indicate the location of outer wall changes, and yellow arrows highlight the extending inner layer contributing to germ tube formation.

Article Snippet: Grids were washed with endotoxin-free water and incubated for 1 h with 100 μg mL -1 recombinant human Fc-Dectin-1 (Fc-hDectin-1a, InvivoGen).

Techniques: Labeling, Synthesized, Staining, Binding Assay

Journal: Advanced Science

Article Title: Clec7a Worsens Long‐Term Outcomes after Ischemic Stroke by Aggravating Microglia‐Mediated Synapse Elimination

doi: 10.1002/advs.202403064

Figure Lengend Snippet: Transcriptome sequencing reveals microglial responses to ischemic stroke. A) Schematic of RNA‐seq analysis of microglia isolated from the ischemic brain 7 days after tMCAO and from sham mice, n = 3 per group, each n consists of 30 mice. B) Principal component analysis (PCA) plot. The two groups of samples were separated when plotting the first (PC1) versus the second component (PC2). C) Scatterplot showing the comparison of log 2 CPM (counts per million) in sham microglia versus tMCAO microglia; red dots represent DAM genes. The orange dashed line indicates a fold change of 1. D) GO analysis of DEGs identified key biological processes in tMCAO microglia compared with sham microglia, which are graphically displayed in bubble plots according to Z scores and significance (log10[adjusted p value]). E–H) Heatmap showing genes related to neuronal death (E), immune response (F), homeostatic state (G) and DAM state (H) in tMCAO microglia versus sham microglia. I) qRT‒PCR analysis showing the expression of phagocytosis‐related genes in isolated microglia from the ischemic penumbra of tMCAO and sham mice, n = 6 per group, each n consists of 3 mice. J) Protein‒protein interaction (PPI) network for microglial phagocytosis‐related genes. K,L). Representative single‐plane images (K) and quantitative analyses (L) of Clec7a (red) in Iba‐1 + microglia (green) in the ischemic penumbra from sham and tMCAO mice. Scale bars, 100 µm. Mice aged 8–10 weeks were used for the experiments shown in this figure. Statistics were derived from 12 slices, n = 4 mice per group. In I and L significance was calculated using two‐tailed unpaired Student's t ‐test. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, and *** p < 0.001.

Article Snippet: The purified human Clec7a protein (Cat. 1859‐DC‐050) and human MD2 protein (Cat. 1787‐MD) were purchased from R&D Systems (USA).

Techniques: Sequencing, RNA Sequencing, Isolation, Comparison, Expressing, Derivative Assay, Two Tailed Test

Journal: Advanced Science

Article Title: Clec7a Worsens Long‐Term Outcomes after Ischemic Stroke by Aggravating Microglia‐Mediated Synapse Elimination

doi: 10.1002/advs.202403064

Figure Lengend Snippet: Clec7a promotes microglia‐mediated synaptic phagocytosis after ischemic stroke. A) Schematic of the experimental design. B) PCR genotyping showed that Clec7a i∆MG (lanes 1, 3, 4, and 6) and WT littermate control (lane 7) mice were successfully generated by crossing Cx3cr1 CreERT2 transgenic mice with Clec7a fl/fl mice. Heterozygotes (Ht) that contained both Clec7a WT and Clec7a flox bands are shown. C) Representative photographs of TTC staining (left) after tMCAO and quantification of the relative infarct volume (right). n = 7 mice per group. D) T2 images at 24 h after the onset of ischemia in both groups. n = 8 mice per group. E) DW images of both groups at 24 h after ischemic stroke. n = 8 mice per group. F) CD68 + lysosome content (green) in Iba‐1 + microglia (red) in the ischemic penumbra from Clec7a i∆MG and Clec7a fl/fl mice subjected to tMCAO. Scale bars, 5 µm. G) Quantification of the lysosomal area relative to the microglial area. H) Representative single‐plane images of Syn and PSD95 staining in the ischemic penumbra. Dotted circles highlight colocalized synapses. Scale bars, 5 µm. I) Quantification of excitatory synapses. J–M) Confocal images and quantification of synaptic puncta engulfed by microglia showing the colocalization of PSD95 (J, K) or Syn (L, M) with CD68 within microglia in the ischemic penumbra from sham and tMCAO mice. The white arrows indicate PSD95 + CD68 + (J) or Syn + CD68 + (L) puncta within microglia. Scale bars, 10 µm. Statistics were derived from 18 slices, n = 6 mice per group. Mice aged 8–10 weeks were used for the experiments shown in this figure. Significance was calculated using either two‐tailed unpaired Student's t ‐test (C–E, G, and I) or one‐way ANOVA, Tukey's multiple comparisons test (K and M). Data are presented as mean ± SD. *** p < 0.001 versus Sham; ## p < 0.01 and ### p < 0.001 versus tMCAO.

Article Snippet: The purified human Clec7a protein (Cat. 1859‐DC‐050) and human MD2 protein (Cat. 1787‐MD) were purchased from R&D Systems (USA).

Techniques: Control, Generated, Transgenic Assay, Staining, Derivative Assay, Two Tailed Test

Journal: Advanced Science

Article Title: Clec7a Worsens Long‐Term Outcomes after Ischemic Stroke by Aggravating Microglia‐Mediated Synapse Elimination

doi: 10.1002/advs.202403064

Figure Lengend Snippet: Inducible knockdown of microglial Clec7a rescues impaired neurological function after ischemic stroke. A–D) Long‐term neurological dysfunction after tMCAO was assessed with the mNSS (A), rotarod test (B), adhesive contact test (C), and adhesive removal test (D). E) Schematic diagram and representative navigation trajectories for learning and memory. F) The swimming speed is presented. G) The average escape latencies. H) The number of entries onto the platform. I) The duration in each zone. J) The number of entries into each zone. n = 10‐13 mice per group. Mice aged 8–10 weeks were used for the experiments shown in this figure. Significance was calculated using either one‐way ANOVA (F and H) or two‐way ANOVA (A‐D, G, and I,J), followed by Tukey's multiple comparisons test. Data are presented as mean ± SD. * p < 0.05, ** p < 0.01, and *** p < 0.001 versus Sham; # p < 0.05, ## p < 0.01, and ### p < 0.001 versus tMCAO; ns indicates no significant difference.

Article Snippet: The purified human Clec7a protein (Cat. 1859‐DC‐050) and human MD2 protein (Cat. 1787‐MD) were purchased from R&D Systems (USA).

Techniques: Knockdown, Adhesive

Journal: Advanced Science

Article Title: Clec7a Worsens Long‐Term Outcomes after Ischemic Stroke by Aggravating Microglia‐Mediated Synapse Elimination

doi: 10.1002/advs.202403064

Figure Lengend Snippet: Microglial Clec7a knockout restores neuronal activity and synaptic transmission after ischemic stroke. A) Representative traces of the action potentials recorded from ischemic penumbra neurons in +180 pA current injection of Clec7a fl/fl and Clec7a i∆MG mice subjected to tMCAO and sham operation. Scale bar, 20 mV, 50 ms. B) Statistics showed that as the injection current increased (from 0 to +360 pA), the number of spikes was significantly increased in tMCAO Clec7a fl/fl mice compared to tMCAO Clec7a i∆MG and sham mice ( Clec7a fl/fl group, n = 16 neurons in 3 mice, Clec7a i∆MG group, n = 16 neurons in 3 mice; Clec7a fl/fl + tMCAO group, n = 22 neurons in 5 mice, Clec7a i∆MG + tMCAO group, n = 24 neurons in 6 mice). C) Representative PPR traces of Clec7a fl/fl and Clec7a i∆MG mice subjected to tMCAO and sham operation after two consecutive stimuli. Scale bar, 100pA, 10 ms. D) Statistical analysis showed that the ratios of tMCAO Clec7a fl/fl mice was increased compared to tMCAO Clec7a i∆MG and sham mice ( Clec7a fl/fl group, n = 10 neurons in 3 mice, Clec7a i∆MG group, n = 12 neurons in 3 mice; Clec7a fl/fl + tMCAO group, n = 12 neurons in 5 mice, Clec7a i∆MG + tMCAO group, n = 16 neurons in 6 mice). Statistical significance was determined by two‐way ANOVA (B) and one‐way ANOVA (D) followed by Tukey's multiple comparisons test. Data are presented as mean ± SD. * p < 0.05 and *** p < 0.001 versus Sham; ### p < 0.001 versus tMCAO.

Article Snippet: The purified human Clec7a protein (Cat. 1859‐DC‐050) and human MD2 protein (Cat. 1787‐MD) were purchased from R&D Systems (USA).

Techniques: Knock-Out, Activity Assay, Transmission Assay, Injection

Journal: Advanced Science

Article Title: Clec7a Worsens Long‐Term Outcomes after Ischemic Stroke by Aggravating Microglia‐Mediated Synapse Elimination

doi: 10.1002/advs.202403064

Figure Lengend Snippet: Clec7a interacts with MD2 in the ischemic brain. A) Immunoprecipitates were subjected to SDS‐PAGE and silver staining. B) Annotated LC–MS/MS spectra of 150‐LGAHLLKIDNSKEFEFIESQTSSHR‐174 from Clec7a and 85‐IELPKRKEVLCHGHDDDYSFCRALK‐109 from MD2 in anti‐Clec7a immunoprecipitates from tMCAO mice. C) Normalized binding curve of Clec7a and MD2. The binding curve yielded a Kd of 2.96 ± 1.11 µ m . The concentration of Clec7a was kept constant at 50 n m while the MD2 concentration was varied from 10 µM to 1.2 nM. n = 3 per group. D) Endogenous Clec7a was coimmunoprecipitated with MD2 after ischemic stroke. The experiments were repeated independently three times. E) The interaction between Clec7a (cyan) and MD2 (pink). The yellow dashed line indicates hydrogen bonding. F) Representative images and analysis of the ischemic penumbra showing the colocalization of MD2 with PSD95, as indicated by the white arrowheads; scale bars, 5 µm. G) Representative images and analysis of the ischemic penumbra showing the colocalization of MD2 with Syn as indicated by the white arrowheads; scale bars, 5 µm. H) Schematic illustrating the in vitro phagocytosis assay in which primary microglia isolated from Clec7a i∆MG or Clec7a fl/fl mice phagocytosed MD2 ko/ko or MD2 wt/wt synaptosomes tagged with pHrodo. I) Representative images of cultured Clec7a i∆MG or Clec7a fl/fl microglia engulfing pHrodo‐conjugated synaptosomes (top: engulfed pHrodo; bottom: merged image of Iba‐1 and pHrodo). Scale bars, 20 µm. Statistics were derived from 18 slices, n = 6 per group. Mice aged 8–10 weeks were used for the experiments shown in this figure. Significance was calculated using either two‐tailed unpaired Student's t ‐test (F and G) or one‐way ANOVA, Tukey's multiple comparisons test (I). Data are presented as mean ± SD. *** p < 0.001.

Article Snippet: The purified human Clec7a protein (Cat. 1859‐DC‐050) and human MD2 protein (Cat. 1787‐MD) were purchased from R&D Systems (USA).

Techniques: SDS Page, Silver Staining, Liquid Chromatography with Mass Spectroscopy, Binding Assay, Concentration Assay, In Vitro, Phagocytosis Assay, Isolation, Cell Culture, Derivative Assay, Two Tailed Test

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Levo-tetrahydropalmatine ameliorates neuropathic pain by inhibiting the activation of the Clec7a-MAPK/NF-κB-NLRP3 inflammasome axis.

doi: 10.1016/j.phymed.2023.155075

Figure Lengend Snippet: Fig. 2. Clec7a-MAPK/NF-κB-NLRP3 Inflammasome Axis might be an effective target of L-THP against NP. (A) Heat maps of DEGs in the CCI group compared with the Sham group (Left) and CCI+l-THP group (Right) by RNA-seq technology (n = 4 rats/group). In clustering analysis, upregulated and downregulated genes are colored red and blue, respectively. (B) Volcano plots of DEGs in the CCI group compared with the Sham group (Left) and CCI+l-THP group (Right). Blue represents downregulated genes; red represents upregulated genes (|Fold change|>1.2, p < 0.05). (C) Venn plots show the total number of identified DEGs in the spinal cord of the Sham, CCI, and CCI+l-THP groups. The overlapped area represented 156 of 636 altered genes in CCI, which were increased by L-THP treatment (Left). The overlapped area represented 24 of 613 altered genes in CCI, which were attenuated by L-THP treatment (Right). (D) qRT-PCR validation profiles of six randomly selected genes. The fold change values of relative expression patterns of different genes are shown on the left Y axis for qRT-PCR, and the FPKM of DEGs were shown on the right Y axis for RNA-seq. (E) The top 20 biological process(BP) terms in the enrichment analysis. (F) 23 enrichment KEGG signaling pathways. (G) Venn diagrams were severally generated by intersecting the DEGs in 3 biological process terms or 4 KEGG pathways related to inflammatory responses.

Article Snippet: First, the Clec7a protein (1859-DC-050, R&D System, USA) was immobilized on the flow cell after being diluted to 30 g/ml in the immobilization buffer (1 PBS-EP, pH 7.4).

Techniques: RNA Sequencing, Quantitative RT-PCR, Biomarker Discovery, Expressing, Protein-Protein interactions, Generated

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Levo-tetrahydropalmatine ameliorates neuropathic pain by inhibiting the activation of the Clec7a-MAPK/NF-κB-NLRP3 inflammasome axis.

doi: 10.1016/j.phymed.2023.155075

Figure Lengend Snippet: Fig. 3. Intragastric administration of L-THP significantly attenuated CCI-induced neuropathic pain by regulating Clec7a-MAPK/NF-κB-NLRP3 inflammasome-induced pyroptosis axis. Pregabalin was used as a positive control drug. (A) Timeline schematic of the experimental paradigm. (B) Repetitive administration of L-THP at 32 and 64 mg/kg at postoperative 6–10 days significantly ameliorated the mechanical withdrawal threshold in the CCI rat model (n = 12 rats/group). (C) qRT-PCR analysis shows the mRNA levels of Clec7a and NLRP3 in the ipsilateral spinal cord of CCI rats on postoperative 10 days(n = 3 rats/group with 3 technical replicates). (D) Protein expressions of Clec7a, p-Syk/Syk, p-NF-κB-p65/NF-κB-p65, p-ERK/ERK, p-JNK/JNK, p-p38/p38 MAPK, NLRP3, GSDMD-N and Caspase-1 in the ipsilateral spinal cord of CCI rats on postoperative 10 days were measured using western blot analysis (n = 3 rats/group with 3 technical replicates). Data are presented as mean ± SEM. Two-way repeated measures ANOVA and Tukey’s post hoc test were used to analyze data at different time points (B). One-way ANOVA was used to analyze data among multiple groups, followed by Tukey’s post hoc test for equal variances or Dunnett’s T3 post hoc test for unequal variances (C-D). **p < 0.01, ***p < 0.001 compared with the Sham group; #p < 0.05, ##p < 0.01, ###p < 0.001 compared with the CCI group; △p < 0.05, △△p < 0.01, △△△p < 0.001 compared with the CCI+l-THP+l group.

Article Snippet: First, the Clec7a protein (1859-DC-050, R&D System, USA) was immobilized on the flow cell after being diluted to 30 g/ml in the immobilization buffer (1 PBS-EP, pH 7.4).

Techniques: Positive Control, Quantitative RT-PCR, Western Blot

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Levo-tetrahydropalmatine ameliorates neuropathic pain by inhibiting the activation of the Clec7a-MAPK/NF-κB-NLRP3 inflammasome axis.

doi: 10.1016/j.phymed.2023.155075

Figure Lengend Snippet: Fig. 5. The overexpression of Clec7a partially inhibits the analgesic effect of L-THP. (A) Timeline schematic of the experimental paradigm. (B) Repetitive administration of L-THP at 64 mg/kg significantly ameliorated the mechanical withdrawal threshold (MWT) in the CCI rat model, while overexpression Clec7a reversed the MWT of CCI rats treated with L-THP (n = 4–10 rats/group). (C) Protein expressions of Clec7a, p-Syk/Syk, p-NF-κB-p65/NF-κB-p65, p-ERK/ERK, p-JNK/ JNK, p-p38/p38 MAPK, NLRP3, GSDMD-N and Caspase-1 in the ipsilateral spinal cord of CCI rats on postoperative 10 days were measured using western blot analysis (n = 3 rats/group with 3 technical replicates). (D) The concentrations of IL-1β and IL-18 in the serum of indicated groups were assessed by ELISA. Data are presented as mean ± SEM. Two-way repeated measures ANOVA and Tukey’s post hoc test were used to analyze data at different time points. One-way ANOVA was used to analyze data among multiple groups, followed by Tukey’s post hoc test for equal variances or Dunnett’s T3 post hoc test for unequal variances (C-D). **p < 0.01, ***p < 0.001 compared with the Sham group; △p < 0.05, △△p < 0.01, △△△p < 0.001 compared with the CCI group; #p < 0.05, ##p < 0.01, ###p < 0.001 compared with the CCI+pLVSO5–NC group; §p < 0.05, §§p < 0.01, §§§p < 0.001 compared with the CCI+pLVSO5–Clec7a group.

Article Snippet: First, the Clec7a protein (1859-DC-050, R&D System, USA) was immobilized on the flow cell after being diluted to 30 g/ml in the immobilization buffer (1 PBS-EP, pH 7.4).

Techniques: Over Expression, Western Blot, Enzyme-linked Immunosorbent Assay

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Levo-tetrahydropalmatine ameliorates neuropathic pain by inhibiting the activation of the Clec7a-MAPK/NF-κB-NLRP3 inflammasome axis.

doi: 10.1016/j.phymed.2023.155075

Figure Lengend Snippet: Fig. 6. L-THP effectively inhibits the upregulation of Clec7a in spinal microglia. Representative images and quantitative analysis of co-localization of Clec7a with Iba-1 (A), GFAP (B) or NeuN (C) in the spinal cord. The tissues were collected from each group of rats on postoperative day 10. White arrows point to Clec7a- positive cells. Scale bars are indicated. Data are presented as mean ± SEM. One-way ANOVA was used to analyze data among multiple groups, followed by Tukey’s post hoc test for equal variances or Dunnett’s T3 post hoc test for unequal variances. *p<0.05, ***p<0.001 compared with the Sham group; ###p < 0.001 compared with the CCI group.

Article Snippet: First, the Clec7a protein (1859-DC-050, R&D System, USA) was immobilized on the flow cell after being diluted to 30 g/ml in the immobilization buffer (1 PBS-EP, pH 7.4).

Techniques:

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Levo-tetrahydropalmatine ameliorates neuropathic pain by inhibiting the activation of the Clec7a-MAPK/NF-κB-NLRP3 inflammasome axis.

doi: 10.1016/j.phymed.2023.155075

Figure Lengend Snippet: Fig. 8. L-THP was directly combined with the Clec7a protein. (A) The schematic diagram of the molecular docking of L-THP with Clec7a, shown as the 3D diagram. The ribbon and stick structure displays the predicted bonds between L-THP and Clec7a. (B) The interaction between L-THP and Clec7a was determined by SPR assay. The equilibrium dissociation constant was evaluated using BIA evaluation software.

Article Snippet: First, the Clec7a protein (1859-DC-050, R&D System, USA) was immobilized on the flow cell after being diluted to 30 g/ml in the immobilization buffer (1 PBS-EP, pH 7.4).

Techniques: SPR Assay, Software

Journal: Phytomedicine : international journal of phytotherapy and phytopharmacology

Article Title: Levo-tetrahydropalmatine ameliorates neuropathic pain by inhibiting the activation of the Clec7a-MAPK/NF-κB-NLRP3 inflammasome axis.

doi: 10.1016/j.phymed.2023.155075

Figure Lengend Snippet: Fig. 9. The graphical abstract illus trates the proposed mechanism un derlying the effect of L-THP in CCI rats. Several pathways, including Clec7a-MAPK/NF-κB-NLRP3 axis, were activated and promoted the release of proinflammatory cytokines that further promoted neuroinflammation and neuropathic pain. L-THP attenuated CCI- induced neuropathic pain through inhibiting the Clec7a-MAPK/NF-κB- NLRP3 signaling pathway, inhibiting the excessive release of proin flammatory cytokines, and decreasing neuroinflammation in the spinal cord.

Article Snippet: First, the Clec7a protein (1859-DC-050, R&D System, USA) was immobilized on the flow cell after being diluted to 30 g/ml in the immobilization buffer (1 PBS-EP, pH 7.4).

Techniques: