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Cell Signaling Technology Inc cb2r
Cb2r, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cb2r/pm41749086-54-38-60
Average 86 stars, based on 1 article reviews

cb2r - by Bioz Stars, 2026-11

86/100 stars

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Article Title: CB2R-mediated GPX4 stabilization: a new avenue for treating cognitive impairment in elderly migraine patients.
Article Snippet: .. Both samples were washed with phosphate-buffered saline (PBS), blocked with 5% bovine serum albumin (BSA) in PBS for 1 h, and incubated at 4 °C overnight with primary antibodies (ionized calcium-binding adapter molecule 1 (IBA-1), GPX4, interleukin-1β (IL-1β), CB2R, calcitonin gene-related peptide (CGRP), C-fos, synaptophysin (SYP), postsynaptic density protein 95 (PSD95), inducible nitric oxide synthase (iNOS), ubiquitin (UB), purchased from Cell Signaling Technology or Santa Cruz) in 3% BSA/PBS. .. After PBS washing, samples were incubated with secondary antibodies (rabbit 488, mouse 555: 1:500; Invitrogen) for 2 h at room temperature, followed by 4’,6-diamidino-2-phenylindole (DAPI) (1:2000; Thermo Fisher) staining for 10 min and PBS washes.

Article Title: CB2R-mediated GPX4 stabilization: a new avenue for treating cognitive impairment in elderly migraine patients
Article Snippet: .. Both samples were washed with phosphate-buffered saline (PBS), blocked with 5% bovine serum albumin (BSA) in PBS for 1 h, and incubated at 4 °C overnight with primary antibodies (ionized calcium-binding adapter molecule 1 (IBA-1), GPX4, interleukin-1β (IL-1β), CB2R, calcitonin gene-related peptide (CGRP), C-fos, synaptophysin (SYP), postsynaptic density protein 95 (PSD95), inducible nitric oxide synthase (iNOS), ubiquitin (UB), purchased from Cell Signaling Technology or Santa Cruz) in 3% BSA/PBS. .. After PBS washing, samples were incubated with secondary antibodies (rabbit 488, mouse 555: 1:500; Invitrogen) for 2 h at room temperature, followed by 4’,6-diamidino-2-phenylindole (DAPI) (1:2000; Thermo Fisher) staining for 10 min and PBS washes.

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Pharmacological CB2R activation mitigates iron overload-induced liver injury, oxidative stress, and inflammation in vivo. a Hepatic Cnr2 mRNA levels determined by qRT-PCR ( n = 6). b Representative Western blot of CB2R protein in the liver, with GAPDH as the loading control. c Representative images of H&E staining (black arrows indicate iron deposition; blue arrows indicate inflammatory cell infiltration) and Masson staining (scale bar = 50 µm). d Serum ALT and AST activities across all experimental groups ( n = 6). e Liver MDA content, SOD activity, and GSH levels indicating oxidative stress and antioxidant status ( n = 6, 6, 3 respectively). f Representative immunofluorescence staining for the macrophage marker F4/80 (green) with DAPI counterstain (blue, scale bar = 20 µm) and corresponding quantification of F4/80 positive cells per unit area ( n = 5). g Relative hepatic mRNA levels of pro-inflammatory cytokines IL-1β , IL-6 , and TNF-α ( n = 5). * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Journal: Molecular Biomedicine

Article Title: Activating Cannabinoid receptor 2 alleviates iron overload-induced liver damage via dual modulation of STAT3/hepcidin and Nrf2/FPN1 pathways

doi: 10.1186/s43556-026-00541-1

Figure Lengend Snippet: Pharmacological CB2R activation mitigates iron overload-induced liver injury, oxidative stress, and inflammation in vivo. a Hepatic Cnr2 mRNA levels determined by qRT-PCR ( n = 6). b Representative Western blot of CB2R protein in the liver, with GAPDH as the loading control. c Representative images of H&E staining (black arrows indicate iron deposition; blue arrows indicate inflammatory cell infiltration) and Masson staining (scale bar = 50 µm). d Serum ALT and AST activities across all experimental groups ( n = 6). e Liver MDA content, SOD activity, and GSH levels indicating oxidative stress and antioxidant status ( n = 6, 6, 3 respectively). f Representative immunofluorescence staining for the macrophage marker F4/80 (green) with DAPI counterstain (blue, scale bar = 20 µm) and corresponding quantification of F4/80 positive cells per unit area ( n = 5). g Relative hepatic mRNA levels of pro-inflammatory cytokines IL-1β , IL-6 , and TNF-α ( n = 5). * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Article Snippet: CB2R antagonist AM630 ( T14204 ) were purchased from TargetMol Chemicals Inc (shanghai, China).

Techniques: Activation Assay, In Vivo, Quantitative RT-PCR, Western Blot, Control, Staining, Activity Assay, Immunofluorescence, Marker

CB2R deficiency exacerbates iron overload-induced liver injury and inflammation. a Representative H&E and Masson staining of liver sections from WT and CB2R-KO mice (scale bar = 50 µm). b Serum ALT and AST activities ( n = 6, 5 respectively). c Liver MDA content ( n = 6). d Representative immunofluorescence staining for F4/80 (scale bar = 20 µm) and corresponding quantification of F4/80 positive cells in WT and CB2R-KO mice ( n = 5). e Relative hepatic mRNA levels of IL-1β , IL-6 , and TNF-α ( n = 5). * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Journal: Molecular Biomedicine

Article Title: Activating Cannabinoid receptor 2 alleviates iron overload-induced liver damage via dual modulation of STAT3/hepcidin and Nrf2/FPN1 pathways

doi: 10.1186/s43556-026-00541-1

Figure Lengend Snippet: CB2R deficiency exacerbates iron overload-induced liver injury and inflammation. a Representative H&E and Masson staining of liver sections from WT and CB2R-KO mice (scale bar = 50 µm). b Serum ALT and AST activities ( n = 6, 5 respectively). c Liver MDA content ( n = 6). d Representative immunofluorescence staining for F4/80 (scale bar = 20 µm) and corresponding quantification of F4/80 positive cells in WT and CB2R-KO mice ( n = 5). e Relative hepatic mRNA levels of IL-1β , IL-6 , and TNF-α ( n = 5). * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Article Snippet: CB2R antagonist AM630 ( T14204 ) were purchased from TargetMol Chemicals Inc (shanghai, China).

Techniques: Staining, Immunofluorescence

Pharmacological CB2R activation limits hepatic iron accumulation by modulating the hepcidin-FPN1 axis. a Representative Prussian blue staining of liver sections from pharmacological treatment groups (black arrows indicate positive blue iron deposits; scale bars = 100 and 20 µm). b Liver iron concentrations quantified using a ferrozine-based assay ( n = 4). c Serum ferritin levels determined using ELISA ( n = 5). d Serum hepcidin levels using ELISA ( n = 6). e Hepatic HAMP mRNA expression determined by qRT-PCR ( n = 5). f Representative Western blots of iron-related proteins FPN1, FTH, and FTL in the liver across different treatment groups, with β-actin as the loading control. * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Journal: Molecular Biomedicine

Article Title: Activating Cannabinoid receptor 2 alleviates iron overload-induced liver damage via dual modulation of STAT3/hepcidin and Nrf2/FPN1 pathways

doi: 10.1186/s43556-026-00541-1

Figure Lengend Snippet: Pharmacological CB2R activation limits hepatic iron accumulation by modulating the hepcidin-FPN1 axis. a Representative Prussian blue staining of liver sections from pharmacological treatment groups (black arrows indicate positive blue iron deposits; scale bars = 100 and 20 µm). b Liver iron concentrations quantified using a ferrozine-based assay ( n = 4). c Serum ferritin levels determined using ELISA ( n = 5). d Serum hepcidin levels using ELISA ( n = 6). e Hepatic HAMP mRNA expression determined by qRT-PCR ( n = 5). f Representative Western blots of iron-related proteins FPN1, FTH, and FTL in the liver across different treatment groups, with β-actin as the loading control. * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Article Snippet: CB2R antagonist AM630 ( T14204 ) were purchased from TargetMol Chemicals Inc (shanghai, China).

Techniques: Activation Assay, Staining, Ferrozine Assay, Enzyme-linked Immunosorbent Assay, Expressing, Quantitative RT-PCR, Western Blot, Control

CB2R deficiency aggravates iron retention while its overexpression alleviates accumulation. a Representative Prussian blue staining of liver sections from WT and CB2R-KO mice (scale bars = 100 and 20 µm). b Liver iron concentrations in WT and CB2R-KO mice ( n = 4). c Serum hepcidin levels ( n = 6). d Hepatic HAMP mRNA expression ( n = 5). e Representative Western blots of FTL and FPN1 in the liver of WT and CB2R-KO mice, with β-actin as the loading control. f Representative Western blot verifying AAV-mediated CB2R overexpression in the liver, with GAPDH as the loading control. g Prussian blue staining of liver sections from AAV-empty and AAV-CB2R injected mice. h Liver iron concentrations following AAV injection ( n = 4). * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Journal: Molecular Biomedicine

Article Title: Activating Cannabinoid receptor 2 alleviates iron overload-induced liver damage via dual modulation of STAT3/hepcidin and Nrf2/FPN1 pathways

doi: 10.1186/s43556-026-00541-1

Figure Lengend Snippet: CB2R deficiency aggravates iron retention while its overexpression alleviates accumulation. a Representative Prussian blue staining of liver sections from WT and CB2R-KO mice (scale bars = 100 and 20 µm). b Liver iron concentrations in WT and CB2R-KO mice ( n = 4). c Serum hepcidin levels ( n = 6). d Hepatic HAMP mRNA expression ( n = 5). e Representative Western blots of FTL and FPN1 in the liver of WT and CB2R-KO mice, with β-actin as the loading control. f Representative Western blot verifying AAV-mediated CB2R overexpression in the liver, with GAPDH as the loading control. g Prussian blue staining of liver sections from AAV-empty and AAV-CB2R injected mice. h Liver iron concentrations following AAV injection ( n = 4). * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Article Snippet: CB2R antagonist AM630 ( T14204 ) were purchased from TargetMol Chemicals Inc (shanghai, China).

Techniques: Over Expression, Staining, Expressing, Western Blot, Control, Injection

CB2R protects against iron-induced toxicity in hepatocytes by suppressing the STAT3/hepcidin pathway. a Immunofluorescence detection of CB2R localisation in liver (green). Nuclear counterstaining was performed with DAPI (blue, Scar bar = 100 and 20 μm). b Cell viability measured by CCK-8 assay across different concentrations of FAC, and comparison between WT and CB2R-KO hepatocytes ( n = 6, 6 respectively). c Representatives of the flurometric assay on MMP and ROS in different treatment groups. d Summarized data demonstrated changes in MMP and ROS in hepatocytes ( n = 3, 5 respectively). e Total cellular iron content ( n = 4). f The level of LIP was detected by using flow cytometry ( n = 5). g HAMP mRNA levels determined by qRT-PCR ( n = 3, 3 respectively). h Representative Western blots of FPN1 protein, with β-actin as the loading control. i Representative Western blots of the upstream regulatory signaling molecules p-SMAD1/5/9, SMAD1/5/9, p-STAT3, and STAT3, with β-actin as the loading control. * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Journal: Molecular Biomedicine

Article Title: Activating Cannabinoid receptor 2 alleviates iron overload-induced liver damage via dual modulation of STAT3/hepcidin and Nrf2/FPN1 pathways

doi: 10.1186/s43556-026-00541-1

Figure Lengend Snippet: CB2R protects against iron-induced toxicity in hepatocytes by suppressing the STAT3/hepcidin pathway. a Immunofluorescence detection of CB2R localisation in liver (green). Nuclear counterstaining was performed with DAPI (blue, Scar bar = 100 and 20 μm). b Cell viability measured by CCK-8 assay across different concentrations of FAC, and comparison between WT and CB2R-KO hepatocytes ( n = 6, 6 respectively). c Representatives of the flurometric assay on MMP and ROS in different treatment groups. d Summarized data demonstrated changes in MMP and ROS in hepatocytes ( n = 3, 5 respectively). e Total cellular iron content ( n = 4). f The level of LIP was detected by using flow cytometry ( n = 5). g HAMP mRNA levels determined by qRT-PCR ( n = 3, 3 respectively). h Representative Western blots of FPN1 protein, with β-actin as the loading control. i Representative Western blots of the upstream regulatory signaling molecules p-SMAD1/5/9, SMAD1/5/9, p-STAT3, and STAT3, with β-actin as the loading control. * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Article Snippet: CB2R antagonist AM630 ( T14204 ) were purchased from TargetMol Chemicals Inc (shanghai, China).

Techniques: Immunofluorescence, CCK-8 Assay, Comparison, Flow Cytometry, Quantitative RT-PCR, Western Blot, Control

CB2R mitigates iron-induced injury in Kupffer cells by promoting Nrf2/FPN1-mediated iron export. a Cell viability of WT and CB2R-KO Kupffer cells exposed to FAC, measured by CCK-8 assay ( n = 6, 6 respectively). b Relative mRNA levels of pro-inflammatory cytokines IL-1β , IL-6 , and TNF-α ( n = 4, 4, 4 respectively). c Representatives of the flurometric assay on MMP and ROS in different treatment groups. d Summarized data demonstrated changes in MMP and ROS in kupffer cells ( n = 3, 5 respectively). e Total cellular iron content ( n = 4). f The level of LIP was detected by using flow cytometry ( n = 4). g Representative Western blots of FPN1 protein in different treatment groups, with β-actin as the loading control. h FPN1 mRNA expression levels determined by qRT-PCR ( n = 4). i Representative Western blots of Nrf2 protein in different treatment groups, with β-actin as the loading control. * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Journal: Molecular Biomedicine

Article Title: Activating Cannabinoid receptor 2 alleviates iron overload-induced liver damage via dual modulation of STAT3/hepcidin and Nrf2/FPN1 pathways

doi: 10.1186/s43556-026-00541-1

Figure Lengend Snippet: CB2R mitigates iron-induced injury in Kupffer cells by promoting Nrf2/FPN1-mediated iron export. a Cell viability of WT and CB2R-KO Kupffer cells exposed to FAC, measured by CCK-8 assay ( n = 6, 6 respectively). b Relative mRNA levels of pro-inflammatory cytokines IL-1β , IL-6 , and TNF-α ( n = 4, 4, 4 respectively). c Representatives of the flurometric assay on MMP and ROS in different treatment groups. d Summarized data demonstrated changes in MMP and ROS in kupffer cells ( n = 3, 5 respectively). e Total cellular iron content ( n = 4). f The level of LIP was detected by using flow cytometry ( n = 4). g Representative Western blots of FPN1 protein in different treatment groups, with β-actin as the loading control. h FPN1 mRNA expression levels determined by qRT-PCR ( n = 4). i Representative Western blots of Nrf2 protein in different treatment groups, with β-actin as the loading control. * P < 0.05, ** P < 0.01, *** P < 0.001. Data are presented as the mean ± SD for each group. Individual data points are displayed as dots

Article Snippet: CB2R antagonist AM630 ( T14204 ) were purchased from TargetMol Chemicals Inc (shanghai, China).

Techniques: CCK-8 Assay, Flow Cytometry, Western Blot, Control, Expressing, Quantitative RT-PCR

Schematic diagram of CB2R-mediated hepatic iron homeostasis. CB2R regulates iron metabolism in hepatocytes and kupffer cells. Iron overload leads to excessive iron deposition in the liver. In hepatocytes, excess iron increases the labile iron pool and ferritin, activates STAT3, and induces hepcidin production, which in turn down-regulates FPN1, exacerbating intracellular iron retention, ROS production, and hepatocyte injury. In Kupffer cells, iron accumulation similarly expands the labile iron pool, promotes M1 polarization and the release of IL-1β, IL-6, and TNF-α, amplifications oxidative stress and inflammatory damage, and drives stellate cell-mediated fibrosis. CB2R activation counteracts these processes by cell type-specific mechanisms: in hepatocytes, CB2R inhibits STAT3-dependent hepcidin induction to preserve FPN1-mediated iron efflux, whereas in Kupffer cells, CB2R enhances Nrf2-driven FPN1 expression, thereby reducing LIP and ROS production. In summary, CB2R signaling coordinates the responses of hepatocytes and macrophages to restore hepatic iron homeostasis and limit liver injury caused by iron overload

Journal: Molecular Biomedicine

Article Title: Activating Cannabinoid receptor 2 alleviates iron overload-induced liver damage via dual modulation of STAT3/hepcidin and Nrf2/FPN1 pathways

doi: 10.1186/s43556-026-00541-1

Figure Lengend Snippet: Schematic diagram of CB2R-mediated hepatic iron homeostasis. CB2R regulates iron metabolism in hepatocytes and kupffer cells. Iron overload leads to excessive iron deposition in the liver. In hepatocytes, excess iron increases the labile iron pool and ferritin, activates STAT3, and induces hepcidin production, which in turn down-regulates FPN1, exacerbating intracellular iron retention, ROS production, and hepatocyte injury. In Kupffer cells, iron accumulation similarly expands the labile iron pool, promotes M1 polarization and the release of IL-1β, IL-6, and TNF-α, amplifications oxidative stress and inflammatory damage, and drives stellate cell-mediated fibrosis. CB2R activation counteracts these processes by cell type-specific mechanisms: in hepatocytes, CB2R inhibits STAT3-dependent hepcidin induction to preserve FPN1-mediated iron efflux, whereas in Kupffer cells, CB2R enhances Nrf2-driven FPN1 expression, thereby reducing LIP and ROS production. In summary, CB2R signaling coordinates the responses of hepatocytes and macrophages to restore hepatic iron homeostasis and limit liver injury caused by iron overload

Article Snippet: CB2R antagonist AM630 ( T14204 ) were purchased from TargetMol Chemicals Inc (shanghai, China).

Techniques: Activation Assay, Expressing

Anti-inflammatory and antipruritic effects of JZL184 are partially mediated by CB2R. ( A ) The flowchart of the AM251, AM630, and JZL184 treatment in IMQ-induced psoriasis model. ( B ) Representative photographs of the dorsal skin and ( C ) H&E staining images of skin lesions on Day 5. ( D ) Epidermal thickness quantified from five randomly selected fields per section for each mouse ( n = 5 mice per group). ( E ) Comparative analysis of PASI scores across groups over the experimental period. The PASI scores were calculated daily from the dorsal neck skin ( n = 5 per group). ( F - G ) Representative photographs of the spleens. Spleen index (mg/g) = spleen weight (mg) ÷ mouse body weight (g) ( n = 5 per group). (H) Scratching bouts recorded over 1 h, measured every other day ( n = 6 per group). Data shown in the graph are presented as mean ± SEM. The P values were calculated by one-way ANOVA and Tukey’stest ( D , G ) or two-way ANOVA and Holm-Šídák test (E, H). * p < 0.05, ** p < 0.01, *** p < 0.001, and ns, not significant when compared. Scale bar = 100 μm

Journal: Inflammation

Article Title: MAGL Inhibition Relieves Psoriasiform Inflammation and Pruritus Via Modulation of ALOX12-12-HETE Axis in Mice

doi: 10.1007/s10753-025-02383-5

Figure Lengend Snippet: Anti-inflammatory and antipruritic effects of JZL184 are partially mediated by CB2R. ( A ) The flowchart of the AM251, AM630, and JZL184 treatment in IMQ-induced psoriasis model. ( B ) Representative photographs of the dorsal skin and ( C ) H&E staining images of skin lesions on Day 5. ( D ) Epidermal thickness quantified from five randomly selected fields per section for each mouse ( n = 5 mice per group). ( E ) Comparative analysis of PASI scores across groups over the experimental period. The PASI scores were calculated daily from the dorsal neck skin ( n = 5 per group). ( F - G ) Representative photographs of the spleens. Spleen index (mg/g) = spleen weight (mg) ÷ mouse body weight (g) ( n = 5 per group). (H) Scratching bouts recorded over 1 h, measured every other day ( n = 6 per group). Data shown in the graph are presented as mean ± SEM. The P values were calculated by one-way ANOVA and Tukey’stest ( D , G ) or two-way ANOVA and Holm-Šídák test (E, H). * p < 0.05, ** p < 0.01, *** p < 0.001, and ns, not significant when compared. Scale bar = 100 μm

Article Snippet: CB2R knockout male mice (strain: B6.129P2-Cnr2 tm1Dgen/J ) of the same age and weight were generated by Jackson Laboratories using ES cell-targeted homologous recombination, resulting in a permanent, global deletion of the Cnr2 gene.

Techniques: Staining

Anti-inflammatory and antipruritic effects of JZL184 in psoriasis are reversed in CB2R−/− mice. ( A - C ) Representative photographs of the dorsal skin and H&E staining images of the skin lesions on Day 5. The epidermal thickness was calculated from five randomly selected fields per section for each mouse ( n = 5 mice per group). ( D , E ) Representative images of the spleens. Spleen index = spleen weight (mg) ÷ mouse body weight (g) ( n = 5 per group). ( F ) Comparative analysis of PASI scores across groups over the full course of the experiment. The PASI scores were assessed daily ( n = 5 per group). ( G ) Scratch bouts in an hour were counted every other day ( n = 5 per group). Data shown in the graph are presented as mean ± SEM. The P values were calculated by one-way ANOVA and Tukey’stest ( C , E ) or two-way ANOVA and Holm-Šídák test ( F , G ). * p < 0.05, ** p < 0.01, *** p < 0.001, and ns, not significant when compared. Scale bar = 100 μm

Journal: Inflammation

Article Title: MAGL Inhibition Relieves Psoriasiform Inflammation and Pruritus Via Modulation of ALOX12-12-HETE Axis in Mice

doi: 10.1007/s10753-025-02383-5

Figure Lengend Snippet: Anti-inflammatory and antipruritic effects of JZL184 in psoriasis are reversed in CB2R−/− mice. ( A - C ) Representative photographs of the dorsal skin and H&E staining images of the skin lesions on Day 5. The epidermal thickness was calculated from five randomly selected fields per section for each mouse ( n = 5 mice per group). ( D , E ) Representative images of the spleens. Spleen index = spleen weight (mg) ÷ mouse body weight (g) ( n = 5 per group). ( F ) Comparative analysis of PASI scores across groups over the full course of the experiment. The PASI scores were assessed daily ( n = 5 per group). ( G ) Scratch bouts in an hour were counted every other day ( n = 5 per group). Data shown in the graph are presented as mean ± SEM. The P values were calculated by one-way ANOVA and Tukey’stest ( C , E ) or two-way ANOVA and Holm-Šídák test ( F , G ). * p < 0.05, ** p < 0.01, *** p < 0.001, and ns, not significant when compared. Scale bar = 100 μm

Techniques: Staining

JZL184 mediates psoriasis-like dermatitis in mice via modulating arachidonic acid metabolism. ( A ) Concentrations of AA in skin lesions detected by UHPLC-MS/MS ( n = 4 per group). ( B ) Heatmap of 50 identified AA metabolites from skin tissues collected 5 days after IMQ treatment. Different samples (shown as columns) with increased or decreased levels of metabolites (shown as rows) are indicated by red or blue. Metabolites are classified into three categories based on the main metabolizing enzymes ( n = 4 per group). ( C - F ) Western blot analysis of ALOX5, ALOX12 and ALOX15 protein in skin tissues, with GAPDH and ACTB as loading controls ( n = 5 per group). ( G ) Representative immunofluorescence images of CB2R + (green) and ALOX12 + (red) cell in skin tissues. The arrows indicated CB2R and ALOX12 double-positive cells. Data shown in the graph are presented as mean ± SEM. The P values were calculated by one-way ANOVA and Tukey’stest ( A , E , F ). * p < 0.05, ** p < 0.01, *** p < 0.001, and ns, not significant when compared. Scale bar = 50 μm

Journal: Inflammation

Article Title: MAGL Inhibition Relieves Psoriasiform Inflammation and Pruritus Via Modulation of ALOX12-12-HETE Axis in Mice

doi: 10.1007/s10753-025-02383-5

Figure Lengend Snippet: JZL184 mediates psoriasis-like dermatitis in mice via modulating arachidonic acid metabolism. ( A ) Concentrations of AA in skin lesions detected by UHPLC-MS/MS ( n = 4 per group). ( B ) Heatmap of 50 identified AA metabolites from skin tissues collected 5 days after IMQ treatment. Different samples (shown as columns) with increased or decreased levels of metabolites (shown as rows) are indicated by red or blue. Metabolites are classified into three categories based on the main metabolizing enzymes ( n = 4 per group). ( C - F ) Western blot analysis of ALOX5, ALOX12 and ALOX15 protein in skin tissues, with GAPDH and ACTB as loading controls ( n = 5 per group). ( G ) Representative immunofluorescence images of CB2R + (green) and ALOX12 + (red) cell in skin tissues. The arrows indicated CB2R and ALOX12 double-positive cells. Data shown in the graph are presented as mean ± SEM. The P values were calculated by one-way ANOVA and Tukey’stest ( A , E , F ). * p < 0.05, ** p < 0.01, *** p < 0.001, and ns, not significant when compared. Scale bar = 50 μm

Techniques: Tandem Mass Spectroscopy, Western Blot, Immunofluorescence

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