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Elabscience Biotechnology mouse tnf α elisa kit

There is a negative correlation between serum MDK levels and BMD. (A) Schematic of the experimental workflow for detecting MDK expression in postmenopausal osteoporosis and in ovariectomized mice. (B) Statistical analysis of T-score differences between hip and lumbar spine BMD in patients (Normal-BMD vs . OP groups). Inter-group comparisons were analyzed by the Wilcoxon signed-rank test. (C) Serum MDK protein concentrations were measured using <t>ELISA.</t> Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). Normal BMD: normal bone mineral density group ( n = 42); OP, osteoporosis group ( n = 42). (D, E) Pearson correlation analysis of the relationship between serum MDK concentration and hip BMD T-score (D) and lumbar BMD T-score (E). (F) Serum MDK protein concentrations in control and OVX mice were measured using ELISA. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (G, H) Detection and quantitative analysis of MDK protein expression in bone sections of control and OVX mice using immunofluorescence. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). Scale bar, 100 μm ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗∗ p < 0.0001.

Mouse Tnf α Elisa Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 95/100, based on 44 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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1) Product Images from "Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression"

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

Journal: Genes & Diseases

doi: 10.1016/j.gendis.2025.101931

Figure Legend Snippet: There is a negative correlation between serum MDK levels and BMD. (A) Schematic of the experimental workflow for detecting MDK expression in postmenopausal osteoporosis and in ovariectomized mice. (B) Statistical analysis of T-score differences between hip and lumbar spine BMD in patients (Normal-BMD vs . OP groups). Inter-group comparisons were analyzed by the Wilcoxon signed-rank test. (C) Serum MDK protein concentrations were measured using ELISA. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). Normal BMD: normal bone mineral density group ( n = 42); OP, osteoporosis group ( n = 42). (D, E) Pearson correlation analysis of the relationship between serum MDK concentration and hip BMD T-score (D) and lumbar BMD T-score (E). (F) Serum MDK protein concentrations in control and OVX mice were measured using ELISA. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (G, H) Detection and quantitative analysis of MDK protein expression in bone sections of control and OVX mice using immunofluorescence. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). Scale bar, 100 μm ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗∗ p < 0.0001.

Techniques Used: Expressing, Enzyme-linked Immunosorbent Assay, Two Tailed Test, Concentration Assay, Control, Immunofluorescence

iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.

Figure Legend Snippet: iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.

Techniques Used: Micro-CT, Staining, Immunohistochemical staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

Schematic representation of MDK alleviating bone loss. MDK is significantly elevated in the serum of postmenopausal osteoporotic women and ovariectomized mice. Due to estrogen deficiency, iMDK alleviates bone loss by promoting bone formation and inhibiting inflammatory factors. Recombinant MDK protein inhibits osteogenic differentiation through the PI3K/AKT signaling pathway and up-regulates inflammatory factors IL-6, TNF-α, and IL-1β via the NF-κB signaling pathway.

Figure Legend Snippet: Schematic representation of MDK alleviating bone loss. MDK is significantly elevated in the serum of postmenopausal osteoporotic women and ovariectomized mice. Due to estrogen deficiency, iMDK alleviates bone loss by promoting bone formation and inhibiting inflammatory factors. Recombinant MDK protein inhibits osteogenic differentiation through the PI3K/AKT signaling pathway and up-regulates inflammatory factors IL-6, TNF-α, and IL-1β via the NF-κB signaling pathway.

Techniques Used: Recombinant

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M2-exo@HI promotes in vitro microglia polarization, BBB repair and neuroprotection. (a) Flow cytometry analysis of M1-type (CD86 + ) and M2-type microglia (CD163 + ) following treatment with different formulations. (b,c) Percentages of CD86 + and CD163 + microglia populations (n = 3). (d–g) The cytokine levels of IL-10, TGF-β, TNF-α, and IL-1β in treated microglia (n = 3). (h) Fluorescence microscopy images showing erythrophagocytosis by microglia across treatment groups. (i) Schematic of the in vitro BBB model assessing FITC-dextran permeability using a transwell assay. (j) Quantitative analysis of FITC-dextran penetration (n = 7). (k) Flow cytometry analysis of neuronal apoptosis across treatments (n = 3). (l) Quantitative analysis of neuronal apoptosis (n = 3). Data are presented as mean ± SD. Statistical significance was tested by one-way ANOVA with Tukey's multiple comparisons test.

Journal: Bioactive Materials

Article Title: M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage

doi: 10.1016/j.bioactmat.2026.01.047

Figure Lengend Snippet: M2-exo@HI promotes in vitro microglia polarization, BBB repair and neuroprotection. (a) Flow cytometry analysis of M1-type (CD86 + ) and M2-type microglia (CD163 + ) following treatment with different formulations. (b,c) Percentages of CD86 + and CD163 + microglia populations (n = 3). (d–g) The cytokine levels of IL-10, TGF-β, TNF-α, and IL-1β in treated microglia (n = 3). (h) Fluorescence microscopy images showing erythrophagocytosis by microglia across treatment groups. (i) Schematic of the in vitro BBB model assessing FITC-dextran permeability using a transwell assay. (j) Quantitative analysis of FITC-dextran penetration (n = 7). (k) Flow cytometry analysis of neuronal apoptosis across treatments (n = 3). (l) Quantitative analysis of neuronal apoptosis (n = 3). Data are presented as mean ± SD. Statistical significance was tested by one-way ANOVA with Tukey's multiple comparisons test.

Article Snippet: ELISA kits included mouse TNF- α ELISA kit (Solarbio), mouse IL-10 ELISA kit (Elabscience), mouse Hp ELISA kit (Elabscience), mouse IL-1β ELISA kit (Solarbio), and TGF-β ELISA kit (Solarbio).

Techniques: In Vitro, Flow Cytometry, Fluorescence, Microscopy, Permeability, Transwell Assay

Journal: Bioactive Materials

Article Title: M2 macrophage-derived exosomes delivering haptoglobin and interleukin-10 plasmids for synergistic therapy of intracerebral hemorrhage

doi: 10.1016/j.bioactmat.2026.01.047

Techniques: In Vitro, Flow Cytometry, Fluorescence, Microscopy, Permeability, Transwell Assay

Journal: Genes & Diseases

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

doi: 10.1016/j.gendis.2025.101931

Figure Lengend Snippet: There is a negative correlation between serum MDK levels and BMD. (A) Schematic of the experimental workflow for detecting MDK expression in postmenopausal osteoporosis and in ovariectomized mice. (B) Statistical analysis of T-score differences between hip and lumbar spine BMD in patients (Normal-BMD vs . OP groups). Inter-group comparisons were analyzed by the Wilcoxon signed-rank test. (C) Serum MDK protein concentrations were measured using ELISA. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). Normal BMD: normal bone mineral density group ( n = 42); OP, osteoporosis group ( n = 42). (D, E) Pearson correlation analysis of the relationship between serum MDK concentration and hip BMD T-score (D) and lumbar BMD T-score (E). (F) Serum MDK protein concentrations in control and OVX mice were measured using ELISA. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). (G, H) Detection and quantitative analysis of MDK protein expression in bone sections of control and OVX mice using immunofluorescence. Inter-group comparisons were analyzed by a two-tailed unpaired Student's t -test (for normally distributed data with equal variance). Scale bar, 100 μm ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗∗ p < 0.0001.

Article Snippet: We purchased the Mouse P1NP (Procollagen 1 N-Terminal Propeptide) ELISA Kit (Cat#e-el-m0233), Mouse IL-6 ELISA Kit (Cat#e-el-m0044), Mouse TNF-α ELISA Kit (Cat#e-el-m3063), and Mouse IL-1β ELISA Kit (Cat#e-el-m0037) from Elabscience (Wuhan, China).

Techniques: Expressing, Enzyme-linked Immunosorbent Assay, Two Tailed Test, Concentration Assay, Control, Immunofluorescence

Journal: Genes & Diseases

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

doi: 10.1016/j.gendis.2025.101931

Figure Lengend Snippet: iMDK alleviates bone loss via dual regulation of bone formation and inflammatory cytokines. (A) Representative micro-CT images of distal femora (top) with three-dimensional reconstruction of the region of interest (bottom), with the blue indicating higher-density bone and the red indicating lower-density bone. (B – D) Statistical quantification of trabecular bone microstructural parameters (BMD, BV/TV, and Tb.Th). Inter-group comparisons were analyzed by one-way ANOVA. (E) Representative images of trabecular bone area in distal femur sections stained with hematoxylin and eosin. Scale bar, 200 μm or 50 μm. (F) Quantitative analysis of the trabecular bone area of the distal femur stained with hematoxylin and eosin. Inter-group comparisons were analyzed by one-way ANOVA. (G) Immunohistochemical staining of OCN in distal femurs. Scale bar, 200 μm or 50 μm. (H) Quantitative analysis of OCN-positive area. Inter-group comparisons were analyzed by one-way ANOVA. (I) Western blotting analysis of inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse bone tissues. (J) Inflammatory cytokine expression (IL-6, TNF-α, and IL-1β) in mouse serum was detected by ELISA. Inter-group comparisons were analyzed by one-way ANOVA. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, and ∗∗∗∗ p < 0.0001; “ns” indicates non-significant differences.

Techniques: Micro-CT, Staining, Immunohistochemical staining, Western Blot, Expressing, Enzyme-linked Immunosorbent Assay

Journal: Genes & Diseases

Article Title: Targeting MDK alleviates bone loss via dual regulation of osteogenic differentiation and inflammatory cytokine expression

doi: 10.1016/j.gendis.2025.101931

Figure Lengend Snippet: Schematic representation of MDK alleviating bone loss. MDK is significantly elevated in the serum of postmenopausal osteoporotic women and ovariectomized mice. Due to estrogen deficiency, iMDK alleviates bone loss by promoting bone formation and inhibiting inflammatory factors. Recombinant MDK protein inhibits osteogenic differentiation through the PI3K/AKT signaling pathway and up-regulates inflammatory factors IL-6, TNF-α, and IL-1β via the NF-κB signaling pathway.

Techniques: Recombinant

BAI increased the cell viability and inhibiting the apoptosis, inflammation, and oxidative stress in ZAS-induced podocyte injury. (A-B) The viability and apoptosis of MPC-5 cells were assessed using CCK-8 (A) and flow cytometry (B) after induction with 10% ZAS for 1 h followed by treatment with 2 µmol/L or 10 µmol/L BAI for 24 h. (C-E) The levels of pro-inflammatory cytokines TNF-α (C), IL-6 (D), and MCP-1 (E) in MPC-5 cells were evaluated by ELISA following treatment with ZAS and BAI. (F) The levels of ROS in MPC-5 cells were evaluated by flow cytometry following treatment with ZAS and BAI. (G-H) The level of T-SOD (G) and MDA (H) in MPC-5 cells were evaluated by ELISA following treatment with ZAS and BAI. Data are represented as mean ± SD ( n = 5 biological repetitions). ns indicated not statistically different, * p < 0.05, ** p < 0. 01, *** p < 0.001.

Journal: Renal Failure

Article Title: Baicalin ameliorates podocyte injury and renal function impairment in idiopathic membranous nephropathy by inhibiting the AGE/RAGE signaling

doi: 10.1080/0886022X.2026.2653954

Figure Lengend Snippet: BAI increased the cell viability and inhibiting the apoptosis, inflammation, and oxidative stress in ZAS-induced podocyte injury. (A-B) The viability and apoptosis of MPC-5 cells were assessed using CCK-8 (A) and flow cytometry (B) after induction with 10% ZAS for 1 h followed by treatment with 2 µmol/L or 10 µmol/L BAI for 24 h. (C-E) The levels of pro-inflammatory cytokines TNF-α (C), IL-6 (D), and MCP-1 (E) in MPC-5 cells were evaluated by ELISA following treatment with ZAS and BAI. (F) The levels of ROS in MPC-5 cells were evaluated by flow cytometry following treatment with ZAS and BAI. (G-H) The level of T-SOD (G) and MDA (H) in MPC-5 cells were evaluated by ELISA following treatment with ZAS and BAI. Data are represented as mean ± SD ( n = 5 biological repetitions). ns indicated not statistically different, * p < 0.05, ** p < 0. 01, *** p < 0.001.

Article Snippet: The ELISA and commercial reagent kits used were as follows: TNF-α ELISA kit (E-EL-M3063, Elabscience), MCP-1 ELISA kit (E-EL-M3001, Elabscience), IL-6 ELISA kit (E-EL-M0044, Elabscience), T-SOD ELISA kit (50104ES60, YEASEN, China), MDA ELISA kit for cells ( GMS50099.1 , AIDISHENG, Jiangsu, China), MDA ELISA kit (GMS50099.2, AIDISHENG), C3 ELISA kit (ADS-0550M1, AIDISHENG), AGE ELISA kit (ab238539, Abcam), and lactate dehydrogenase (LDH) activity assay kit (E-BC-K046-M, Elabscience).

Techniques: CCK-8 Assay, Flow Cytometry, Enzyme-linked Immunosorbent Assay

BAI protected the renal function of mice against IMN. After being treated with 20 mg/kg and 100 mg/kg BAI, (A-B) the levels of total protein (A) and albumin (B) in the serum of mouse were measured using biochemical analysis. (C) The level of serum C3 in mouse was determined using ELISA assay. (D-E) The levels of BUN (D) and Scr (E) in IMN mice serum were measured using biochemical analysis. (F) The urine protein of IMN mice was determined using biochemical analysis. Data are represented as mean ± SD ( n = 8 biological repetitions). ns indicated not statistically different, * p < 0.05, ** p < 0. 01, *** p < 0.001.

Journal: Renal Failure

Article Title: Baicalin ameliorates podocyte injury and renal function impairment in idiopathic membranous nephropathy by inhibiting the AGE/RAGE signaling

doi: 10.1080/0886022X.2026.2653954

Figure Lengend Snippet: BAI protected the renal function of mice against IMN. After being treated with 20 mg/kg and 100 mg/kg BAI, (A-B) the levels of total protein (A) and albumin (B) in the serum of mouse were measured using biochemical analysis. (C) The level of serum C3 in mouse was determined using ELISA assay. (D-E) The levels of BUN (D) and Scr (E) in IMN mice serum were measured using biochemical analysis. (F) The urine protein of IMN mice was determined using biochemical analysis. Data are represented as mean ± SD ( n = 8 biological repetitions). ns indicated not statistically different, * p < 0.05, ** p < 0. 01, *** p < 0.001.

Techniques: Enzyme-linked Immunosorbent Assay

BAI mitigated the inflammation of IMN mice. (A) After being treated with 20 mg/kg and 100 mg/kg BAI, the histopathology in kidney tissue of IMN mice was determined using HE staining. (B) After being treated with BAI, the level of CD68-positive cells in the kidney tissue of IMN mice was determined using IHC. (C-E) After being treated with BAI, the serum levels of TNF-α (C), IL-6 (D), and MCP-1 (E) in IMN mice were detected using ELISA. Data are represented as mean ± SD ( n = 8 biological repetitions). * p < 0.05, ** p < 0. 01, *** p < 0.001.

Journal: Renal Failure

Article Title: Baicalin ameliorates podocyte injury and renal function impairment in idiopathic membranous nephropathy by inhibiting the AGE/RAGE signaling

doi: 10.1080/0886022X.2026.2653954

Figure Lengend Snippet: BAI mitigated the inflammation of IMN mice. (A) After being treated with 20 mg/kg and 100 mg/kg BAI, the histopathology in kidney tissue of IMN mice was determined using HE staining. (B) After being treated with BAI, the level of CD68-positive cells in the kidney tissue of IMN mice was determined using IHC. (C-E) After being treated with BAI, the serum levels of TNF-α (C), IL-6 (D), and MCP-1 (E) in IMN mice were detected using ELISA. Data are represented as mean ± SD ( n = 8 biological repetitions). * p < 0.05, ** p < 0. 01, *** p < 0.001.

Techniques: Histopathology, Staining, Enzyme-linked Immunosorbent Assay

BAI mitigated oxidative stress of IMN mice. (A) After being treated with BAI, the ROS level in the kidney tissue of IMN mice was determined using flow cytometry. (B) After being treated with BAI, the LDH level in kidney tissue of IMN mice was detected using a commercial reagent kit. (C-D) After being treated with BAI, the levels of T-SOD (C) and MDA (D) in kidney tissue of IMN mice was detected by ELISA. Data are represented as mean ± SD ( n = 8 biological repetitions). *** p < 0.001.

Journal: Renal Failure

Article Title: Baicalin ameliorates podocyte injury and renal function impairment in idiopathic membranous nephropathy by inhibiting the AGE/RAGE signaling

doi: 10.1080/0886022X.2026.2653954

Figure Lengend Snippet: BAI mitigated oxidative stress of IMN mice. (A) After being treated with BAI, the ROS level in the kidney tissue of IMN mice was determined using flow cytometry. (B) After being treated with BAI, the LDH level in kidney tissue of IMN mice was detected using a commercial reagent kit. (C-D) After being treated with BAI, the levels of T-SOD (C) and MDA (D) in kidney tissue of IMN mice was detected by ELISA. Data are represented as mean ± SD ( n = 8 biological repetitions). *** p < 0.001.

Techniques: Flow Cytometry, Enzyme-linked Immunosorbent Assay

BAI suppressed the inflammation and oxidative stress of ZAS-induced podocytes by inactivating the AGE/RAGE pathway. (A-B) After being 10% ZAS induced for 1 h and 2 µmol/L BAI treated for 24 h, the expression of AGE (A) and RAGE (B) in MPC-5 cells were quantified. (C) After being treated with 2 µmol/L BAI and 2 µg/mL AGE-BSA for 24 h, the expression of RAGE in ZAS-induced MPC-5 cells were quantified using western blot assay. (D) The viability of ZAS-induced MPC-5 cells after BAI and AGE-BSA treatment was determined using CCK-8 assay. (E-G) The levels of pro-inflammatory cytokines TNF-α (E), IL-6 (F), and MCP-1 (G) in ZAS-induced MPC-5 cells after BAI and AGE-BSA treatment were evaluated by ELISA. (H-I) The level of T-SOD (H) and MDA (I) in ZAS-induced MPC-5 cells after BAI and AGE-BSA treatment were evaluated by ELISA. Data are represented as mean ± SD ( n = 5 biological repetitions). ns indicated not statistically different, * p < 0.05, ** p < 0. 01, *** p < 0.001.

Journal: Renal Failure

Article Title: Baicalin ameliorates podocyte injury and renal function impairment in idiopathic membranous nephropathy by inhibiting the AGE/RAGE signaling

doi: 10.1080/0886022X.2026.2653954

Figure Lengend Snippet: BAI suppressed the inflammation and oxidative stress of ZAS-induced podocytes by inactivating the AGE/RAGE pathway. (A-B) After being 10% ZAS induced for 1 h and 2 µmol/L BAI treated for 24 h, the expression of AGE (A) and RAGE (B) in MPC-5 cells were quantified. (C) After being treated with 2 µmol/L BAI and 2 µg/mL AGE-BSA for 24 h, the expression of RAGE in ZAS-induced MPC-5 cells were quantified using western blot assay. (D) The viability of ZAS-induced MPC-5 cells after BAI and AGE-BSA treatment was determined using CCK-8 assay. (E-G) The levels of pro-inflammatory cytokines TNF-α (E), IL-6 (F), and MCP-1 (G) in ZAS-induced MPC-5 cells after BAI and AGE-BSA treatment were evaluated by ELISA. (H-I) The level of T-SOD (H) and MDA (I) in ZAS-induced MPC-5 cells after BAI and AGE-BSA treatment were evaluated by ELISA. Data are represented as mean ± SD ( n = 5 biological repetitions). ns indicated not statistically different, * p < 0.05, ** p < 0. 01, *** p < 0.001.

Techniques: Expressing, Western Blot, CCK-8 Assay, Enzyme-linked Immunosorbent Assay

BAI protected the renal function of mice against IMN by inactivating the AGE/RAGE pathway. (A) After being treated with 20 mg/kg BAI and 20 mg/kg AGE-BSA, the expression of RAGE in mouse kidney tissues were determined using western blot assay. (B-C) The levels of total protein (B) and albumin (C) in IMN mice serum was measured using biochemical analysis. (D) The level of serum C3 in IMN mice was determined using ELISA assay. (E-F) The levels of BUN (E) and Scr (F) in IMN mice serum was measured using biochemical analysis. (G) The level of urine protein in IMN mice was determined using biochemical analysis. Data are represented as mean ± SD ( n = 8 biological repetitions). ns indicated not statistically different, * p < 0.05, ** p < 0. 01, *** p < 0.001.

Journal: Renal Failure

Article Title: Baicalin ameliorates podocyte injury and renal function impairment in idiopathic membranous nephropathy by inhibiting the AGE/RAGE signaling

doi: 10.1080/0886022X.2026.2653954

Figure Lengend Snippet: BAI protected the renal function of mice against IMN by inactivating the AGE/RAGE pathway. (A) After being treated with 20 mg/kg BAI and 20 mg/kg AGE-BSA, the expression of RAGE in mouse kidney tissues were determined using western blot assay. (B-C) The levels of total protein (B) and albumin (C) in IMN mice serum was measured using biochemical analysis. (D) The level of serum C3 in IMN mice was determined using ELISA assay. (E-F) The levels of BUN (E) and Scr (F) in IMN mice serum was measured using biochemical analysis. (G) The level of urine protein in IMN mice was determined using biochemical analysis. Data are represented as mean ± SD ( n = 8 biological repetitions). ns indicated not statistically different, * p < 0.05, ** p < 0. 01, *** p < 0.001.

Techniques: Expressing, Western Blot, Enzyme-linked Immunosorbent Assay

BAI mitigated the inflammation and oxidative stress of IMN mice via AGE/RAGE pathway. (A) After being treated with 20 mg/kg BAI and 20 mg/kg AGE-BSA, the histopathology in kidney tissue of IMN mice was determined using HE staining. (B) The level of CD68-positive cells in the kidney tissue of IMN mice was determined using IHC. (C-E) The serum levels of TNF-α (C), IL-6 (D), and MCP-1 (E) in IMN mice were detected using ELISA. (F) The LDH level in the kidney tissue of IMN mice was detected using a commercial reagent kit. (G-H) The levels of T-SOD (G) and MDA (H) in kidney tissue of IMN mice was detected by ELISA. Data are represented as mean ± SD ( n = 8 biological repetitions). ** p < 0.01, *** p < 0.001.

Journal: Renal Failure

Article Title: Baicalin ameliorates podocyte injury and renal function impairment in idiopathic membranous nephropathy by inhibiting the AGE/RAGE signaling

doi: 10.1080/0886022X.2026.2653954

Figure Lengend Snippet: BAI mitigated the inflammation and oxidative stress of IMN mice via AGE/RAGE pathway. (A) After being treated with 20 mg/kg BAI and 20 mg/kg AGE-BSA, the histopathology in kidney tissue of IMN mice was determined using HE staining. (B) The level of CD68-positive cells in the kidney tissue of IMN mice was determined using IHC. (C-E) The serum levels of TNF-α (C), IL-6 (D), and MCP-1 (E) in IMN mice were detected using ELISA. (F) The LDH level in the kidney tissue of IMN mice was detected using a commercial reagent kit. (G-H) The levels of T-SOD (G) and MDA (H) in kidney tissue of IMN mice was detected by ELISA. Data are represented as mean ± SD ( n = 8 biological repetitions). ** p < 0.01, *** p < 0.001.

Techniques: Histopathology, Staining, Enzyme-linked Immunosorbent Assay

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