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AA exacerbated podocyte injury in PAN‐induced rats. Eight‐week‐old male Sprague–Dawley rats (180–200 g) were subjected to puromycin aminonucleoside (PAN)‐induced podocyte injury by a single intraperitoneal injection of PAN (7 mg/100 g body weight). Ten days after PAN injection, rats in the PAN+AA group received arachidonic acid (AA, 3 mg/kg, i.p.) to evaluate AA‐associated exacerbation of established PAN‐induced injury. (A) Serum AA levels were measured by <t>ELISA.</t> Serum albumin, serum creatinine, 24‐h urinary albumin, serum cholesterol and serum triglyceride levels were measured as indicators of renal function and metabolic status ( n = 6). (B) Representative haematoxylin and eosin (H&E), Masson's trichrome, and periodic acid‐Schiff (PAS) staining of kidney sections ( n = 6). Scale bar, 20 μm. (C) Representative transmission electron microscopy images of podocyte foot processes and quantitative analysis of glomerular basement membrane (GBM) thickness, foot‐process width, and the number of foot processes per μm GBM ( n = 3). Scale bar, 5.0 μm. (D) Representative immunofluorescence staining of nephrin in glomeruli. Nephrin is shown in red and nuclei are counterstained with DAPI in blue ( n = 6). Scale bar, 20 μm. (E) Representative Western blot analysis and quantification of nephrin protein expression in renal tissue lysates ( n = 6). Data are expressed as the mean ± SD and analysed by one‐way ANOVA with Bonferroni correction. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant. AA, arachidonic acid; GBM, glomerular basement membrane; i.p., intraperitoneal; MCD, minimal change disease; PAN, puromycin aminonucleoside.
Immunosorbent Assay Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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AA exacerbated podocyte injury in PAN‐induced rats. Eight‐week‐old male Sprague–Dawley rats (180–200 g) were subjected to puromycin aminonucleoside (PAN)‐induced podocyte injury by a single intraperitoneal injection of PAN (7 mg/100 g body weight). Ten days after PAN injection, rats in the PAN+AA group received arachidonic acid (AA, 3 mg/kg, i.p.) to evaluate AA‐associated exacerbation of established PAN‐induced injury. (A) Serum AA levels were measured by <t>ELISA.</t> Serum albumin, serum creatinine, 24‐h urinary albumin, serum cholesterol and serum triglyceride levels were measured as indicators of renal function and metabolic status ( n = 6). (B) Representative haematoxylin and eosin (H&E), Masson's trichrome, and periodic acid‐Schiff (PAS) staining of kidney sections ( n = 6). Scale bar, 20 μm. (C) Representative transmission electron microscopy images of podocyte foot processes and quantitative analysis of glomerular basement membrane (GBM) thickness, foot‐process width, and the number of foot processes per μm GBM ( n = 3). Scale bar, 5.0 μm. (D) Representative immunofluorescence staining of nephrin in glomeruli. Nephrin is shown in red and nuclei are counterstained with DAPI in blue ( n = 6). Scale bar, 20 μm. (E) Representative Western blot analysis and quantification of nephrin protein expression in renal tissue lysates ( n = 6). Data are expressed as the mean ± SD and analysed by one‐way ANOVA with Bonferroni correction. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant. AA, arachidonic acid; GBM, glomerular basement membrane; i.p., intraperitoneal; MCD, minimal change disease; PAN, puromycin aminonucleoside.
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enzyme linked immunosorbent assay kit  (Elabscience Biotechnology)
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Elabscience Biotechnology enzyme linked immunosorbent assay kit
AA exacerbated podocyte injury in PAN‐induced rats. Eight‐week‐old male Sprague–Dawley rats (180–200 g) were subjected to puromycin aminonucleoside (PAN)‐induced podocyte injury by a single intraperitoneal injection of PAN (7 mg/100 g body weight). Ten days after PAN injection, rats in the PAN+AA group received arachidonic acid (AA, 3 mg/kg, i.p.) to evaluate AA‐associated exacerbation of established PAN‐induced injury. (A) Serum AA levels were measured by <t>ELISA.</t> Serum albumin, serum creatinine, 24‐h urinary albumin, serum cholesterol and serum triglyceride levels were measured as indicators of renal function and metabolic status ( n = 6). (B) Representative haematoxylin and eosin (H&E), Masson's trichrome, and periodic acid‐Schiff (PAS) staining of kidney sections ( n = 6). Scale bar, 20 μm. (C) Representative transmission electron microscopy images of podocyte foot processes and quantitative analysis of glomerular basement membrane (GBM) thickness, foot‐process width, and the number of foot processes per μm GBM ( n = 3). Scale bar, 5.0 μm. (D) Representative immunofluorescence staining of nephrin in glomeruli. Nephrin is shown in red and nuclei are counterstained with DAPI in blue ( n = 6). Scale bar, 20 μm. (E) Representative Western blot analysis and quantification of nephrin protein expression in renal tissue lysates ( n = 6). Data are expressed as the mean ± SD and analysed by one‐way ANOVA with Bonferroni correction. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant. AA, arachidonic acid; GBM, glomerular basement membrane; i.p., intraperitoneal; MCD, minimal change disease; PAN, puromycin aminonucleoside.
Enzyme Linked Immunosorbent Assay Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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enzyme linked immunosorbent assay elisa  (Elabscience Biotechnology)
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AA exacerbated podocyte injury in PAN‐induced rats. Eight‐week‐old male Sprague–Dawley rats (180–200 g) were subjected to puromycin aminonucleoside (PAN)‐induced podocyte injury by a single intraperitoneal injection of PAN (7 mg/100 g body weight). Ten days after PAN injection, rats in the PAN+AA group received arachidonic acid (AA, 3 mg/kg, i.p.) to evaluate AA‐associated exacerbation of established PAN‐induced injury. (A) Serum AA levels were measured by <t>ELISA.</t> Serum albumin, serum creatinine, 24‐h urinary albumin, serum cholesterol and serum triglyceride levels were measured as indicators of renal function and metabolic status ( n = 6). (B) Representative haematoxylin and eosin (H&E), Masson's trichrome, and periodic acid‐Schiff (PAS) staining of kidney sections ( n = 6). Scale bar, 20 μm. (C) Representative transmission electron microscopy images of podocyte foot processes and quantitative analysis of glomerular basement membrane (GBM) thickness, foot‐process width, and the number of foot processes per μm GBM ( n = 3). Scale bar, 5.0 μm. (D) Representative immunofluorescence staining of nephrin in glomeruli. Nephrin is shown in red and nuclei are counterstained with DAPI in blue ( n = 6). Scale bar, 20 μm. (E) Representative Western blot analysis and quantification of nephrin protein expression in renal tissue lysates ( n = 6). Data are expressed as the mean ± SD and analysed by one‐way ANOVA with Bonferroni correction. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant. AA, arachidonic acid; GBM, glomerular basement membrane; i.p., intraperitoneal; MCD, minimal change disease; PAN, puromycin aminonucleoside.
Enzyme Linked Immunosorbent Assay Elisa, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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AA exacerbated podocyte injury in PAN‐induced rats. Eight‐week‐old male Sprague–Dawley rats (180–200 g) were subjected to puromycin aminonucleoside (PAN)‐induced podocyte injury by a single intraperitoneal injection of PAN (7 mg/100 g body weight). Ten days after PAN injection, rats in the PAN+AA group received arachidonic acid (AA, 3 mg/kg, i.p.) to evaluate AA‐associated exacerbation of established PAN‐induced injury. (A) Serum AA levels were measured by <t>ELISA.</t> Serum albumin, serum creatinine, 24‐h urinary albumin, serum cholesterol and serum triglyceride levels were measured as indicators of renal function and metabolic status ( n = 6). (B) Representative haematoxylin and eosin (H&E), Masson's trichrome, and periodic acid‐Schiff (PAS) staining of kidney sections ( n = 6). Scale bar, 20 μm. (C) Representative transmission electron microscopy images of podocyte foot processes and quantitative analysis of glomerular basement membrane (GBM) thickness, foot‐process width, and the number of foot processes per μm GBM ( n = 3). Scale bar, 5.0 μm. (D) Representative immunofluorescence staining of nephrin in glomeruli. Nephrin is shown in red and nuclei are counterstained with DAPI in blue ( n = 6). Scale bar, 20 μm. (E) Representative Western blot analysis and quantification of nephrin protein expression in renal tissue lysates ( n = 6). Data are expressed as the mean ± SD and analysed by one‐way ANOVA with Bonferroni correction. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant. AA, arachidonic acid; GBM, glomerular basement membrane; i.p., intraperitoneal; MCD, minimal change disease; PAN, puromycin aminonucleoside.
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Skin-tissue <t> IL-22 </t> concentrations across the experimental groups.
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Skin-tissue <t> IL-22 </t> concentrations across the experimental groups.
Enzyme Linked Immunosorbent Assay Elisa Kits, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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AA exacerbated podocyte injury in PAN‐induced rats. Eight‐week‐old male Sprague–Dawley rats (180–200 g) were subjected to puromycin aminonucleoside (PAN)‐induced podocyte injury by a single intraperitoneal injection of PAN (7 mg/100 g body weight). Ten days after PAN injection, rats in the PAN+AA group received arachidonic acid (AA, 3 mg/kg, i.p.) to evaluate AA‐associated exacerbation of established PAN‐induced injury. (A) Serum AA levels were measured by ELISA. Serum albumin, serum creatinine, 24‐h urinary albumin, serum cholesterol and serum triglyceride levels were measured as indicators of renal function and metabolic status ( n = 6). (B) Representative haematoxylin and eosin (H&E), Masson's trichrome, and periodic acid‐Schiff (PAS) staining of kidney sections ( n = 6). Scale bar, 20 μm. (C) Representative transmission electron microscopy images of podocyte foot processes and quantitative analysis of glomerular basement membrane (GBM) thickness, foot‐process width, and the number of foot processes per μm GBM ( n = 3). Scale bar, 5.0 μm. (D) Representative immunofluorescence staining of nephrin in glomeruli. Nephrin is shown in red and nuclei are counterstained with DAPI in blue ( n = 6). Scale bar, 20 μm. (E) Representative Western blot analysis and quantification of nephrin protein expression in renal tissue lysates ( n = 6). Data are expressed as the mean ± SD and analysed by one‐way ANOVA with Bonferroni correction. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant. AA, arachidonic acid; GBM, glomerular basement membrane; i.p., intraperitoneal; MCD, minimal change disease; PAN, puromycin aminonucleoside.

Journal: Journal of Cellular and Molecular Medicine

Article Title: Arachidonic Acid Disrupts PKM2 ‐Linked Glycolysis‐Related Metabolism and Exacerbates PAN ‐Induced Podocyte Injury

doi: 10.1111/jcmm.71404

Figure Lengend Snippet: AA exacerbated podocyte injury in PAN‐induced rats. Eight‐week‐old male Sprague–Dawley rats (180–200 g) were subjected to puromycin aminonucleoside (PAN)‐induced podocyte injury by a single intraperitoneal injection of PAN (7 mg/100 g body weight). Ten days after PAN injection, rats in the PAN+AA group received arachidonic acid (AA, 3 mg/kg, i.p.) to evaluate AA‐associated exacerbation of established PAN‐induced injury. (A) Serum AA levels were measured by ELISA. Serum albumin, serum creatinine, 24‐h urinary albumin, serum cholesterol and serum triglyceride levels were measured as indicators of renal function and metabolic status ( n = 6). (B) Representative haematoxylin and eosin (H&E), Masson's trichrome, and periodic acid‐Schiff (PAS) staining of kidney sections ( n = 6). Scale bar, 20 μm. (C) Representative transmission electron microscopy images of podocyte foot processes and quantitative analysis of glomerular basement membrane (GBM) thickness, foot‐process width, and the number of foot processes per μm GBM ( n = 3). Scale bar, 5.0 μm. (D) Representative immunofluorescence staining of nephrin in glomeruli. Nephrin is shown in red and nuclei are counterstained with DAPI in blue ( n = 6). Scale bar, 20 μm. (E) Representative Western blot analysis and quantification of nephrin protein expression in renal tissue lysates ( n = 6). Data are expressed as the mean ± SD and analysed by one‐way ANOVA with Bonferroni correction. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant. AA, arachidonic acid; GBM, glomerular basement membrane; i.p., intraperitoneal; MCD, minimal change disease; PAN, puromycin aminonucleoside.

Article Snippet: Serum arachidonic acid (AA) levels were measured using a commercially available enzyme‐linked immunosorbent assay (ELISA) kit (Elabscience, catalogue no. E‐EL‐0051) according to the manufacturer's instructions.

Techniques: Injection, Enzyme-linked Immunosorbent Assay, Staining, Transmission Assay, Electron Microscopy, Analysis, Membrane, Immunofluorescence, Western Blot, Expressing, Tissue

Skin-tissue IL-22 concentrations across the experimental groups.

Journal: Frontiers in Medicine

Article Title: Effects of topical Averrhoa bilimbi leaf extract cream on IL-22 and filaggrin in a murine model of atopic dermatitis

doi: 10.3389/fmed.2026.1883375

Figure Lengend Snippet: Skin-tissue IL-22 concentrations across the experimental groups.

Article Snippet: Cutaneous IL-22 concentrations were quantified using a mouse IL-22 enzyme-linked immunosorbent assay kit (Elabscience, catalog no. E-EL-M2446, Wuhan, China) according to the manufacturer's instructions.

Techniques: Control, Positive Control

Skin-tissue IL-22 concentrations after topical administration of A. bilimbi leaf extract cream in a mouse model of atopic dermatitis.

Journal: Frontiers in Medicine

Article Title: Effects of topical Averrhoa bilimbi leaf extract cream on IL-22 and filaggrin in a murine model of atopic dermatitis

doi: 10.3389/fmed.2026.1883375

Figure Lengend Snippet: Skin-tissue IL-22 concentrations after topical administration of A. bilimbi leaf extract cream in a mouse model of atopic dermatitis.

Article Snippet: Cutaneous IL-22 concentrations were quantified using a mouse IL-22 enzyme-linked immunosorbent assay kit (Elabscience, catalog no. E-EL-M2446, Wuhan, China) according to the manufacturer's instructions.

Techniques: Tissue, Cream

Post-hoc Dunn test with Benjamini–Hochberg FDR correction for IL-22 levels.

Journal: Frontiers in Medicine

Article Title: Effects of topical Averrhoa bilimbi leaf extract cream on IL-22 and filaggrin in a murine model of atopic dermatitis

doi: 10.3389/fmed.2026.1883375

Figure Lengend Snippet: Post-hoc Dunn test with Benjamini–Hochberg FDR correction for IL-22 levels.

Article Snippet: Cutaneous IL-22 concentrations were quantified using a mouse IL-22 enzyme-linked immunosorbent assay kit (Elabscience, catalog no. E-EL-M2446, Wuhan, China) according to the manufacturer's instructions.

Techniques: Comparison, Positive Control, Control