adiponectin mouse elisa  (BioVendor Instruments)

Journal: Journal of Diabetes Investigation

Article Title: NSUN2 ‐mediated m 5 C methylation modification regulates trophoblast cell proliferation, apoptosis, and autophagy in gestational diabetes mellitus

doi: 10.1111/jdi.70140

Figure Lengend Snippet: NSUN2‐mediated m 5 C modification inhibited cell proliferation and promoted apoptosis, inflammation, and autophagy in HG‐treated HTR‐8/SVneo cells. (a, b) NSUN2 expression was analyzed by RT‐qPCR and Western blot after shNSUN2 transfection; (c) CCK‐8 was used to detect the cell viability in each group; (d, e) EdU was performed to analyze cell proliferation in each group; (f, g) the apoptosis rate in each group was analyzed by flow cytometry; (h, i) ELISA was performed to analyze the contents of TNF‐α and IL‐1β in each group; (j) Western blot was used to evaluate autophagy‐related protein levels in each group. All experiments were performed with three independent biological replicates ( N = 3), each measured in triplicate. Data are presented as mean ± SD. Student's t ‐test (a, b) or one‐way anova (c–j) was used for statistical analysis. CCK‐8, cell counting kit‐8; EdU, ethynyldeoxyuridine; ELISA, enzyme‐linked immunosorbent assay; IL, interleukin; NSUN, NOL1/NOP2/SUN domain; RT‐qPCR, reverse transcription‐polymerase chain reaction; TNF, tumor necrosis factor.

Article Snippet: TNF‐α, IL‐1β, insulin, and adiponectin concentrations in mouse serum were quantified using ELISA kits (CUSABIO) according to the manufacturer's protocol.

Techniques: Modification, Expressing, Quantitative RT-PCR, Western Blot, Transfection, CCK-8 Assay, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Cell Counting, Reverse Transcription, Polymerase Chain Reaction

Journal: Journal of Diabetes Investigation

Article Title: NSUN2 ‐mediated m 5 C methylation modification regulates trophoblast cell proliferation, apoptosis, and autophagy in gestational diabetes mellitus

doi: 10.1111/jdi.70140

Figure Lengend Snippet: PINK1 inhibition increased cell proliferation and suppressed apoptosis, inflammation, and autophagy in HG‐treated HTR‐8/SVneo cells. (a, b) PINK1 mRNA and protein levels were analyzed by RT‐qPCR and Western blot after PINK1 deficiency; cell viability and proliferation in each group were assessed using (c) CCK‐8 and (d, e) EdU assays; (f, g) flow cytometry was performed to detect the apoptosis rate in each group; (h, i) ELISA was performed to analyze the contents of TNF‐α and IL‐1β in each group; (j) Western blot was used to evaluate autophagy‐related protein levels in each group. All experiments were performed with three independent biological replicates ( N = 3), each measured in triplicate. Student's t ‐test (a, b) or one‐way anova (c–j) was used for statistical analysis. CCK‐8, cell counting kit‐8; EdU, ethynyldeoxyuridine; ELISA, enzyme‐linked immunosorbent assay; IL, interleukin; PINK1, PTEN‐induced putative kinase 1; RT‐qPCR, reverse transcription‐polymerase chain reaction; TNF, tumor necrosis factor.

Article Snippet: TNF‐α, IL‐1β, insulin, and adiponectin concentrations in mouse serum were quantified using ELISA kits (CUSABIO) according to the manufacturer's protocol.

Techniques: Inhibition, Quantitative RT-PCR, Western Blot, CCK-8 Assay, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Cell Counting, Reverse Transcription, Polymerase Chain Reaction

Journal: Journal of Diabetes Investigation

Article Title: NSUN2 ‐mediated m 5 C methylation modification regulates trophoblast cell proliferation, apoptosis, and autophagy in gestational diabetes mellitus

doi: 10.1111/jdi.70140

Figure Lengend Snippet: PINK1 overexpression decreased cell proliferation and promoted apoptosis, inflammation, and autophagy in HG‐treated HTR‐8/SVneo cells. (a, b) RT‐qPCR and Western blot were used to measure the mRNA and protein levels of PINK1 after PINK1 overexpression; (c) CCK‐8 assay was employed to assess the cell viability in each group; (d, e) cell proliferation of HTR‐8/SVneo cells in each group was evaluated by EdU assay; (f, g) flow cytometry was performed to detect the apoptosis rate in each group; (h, i) ELISA was performed to analyze the contents of TNF‐α and IL‐1β in each group; (j) Western blot was used to evaluate autophagy‐related protein levels in each group. All experiments were performed with three independent biological replicates ( N = 3), each measured in triplicate. Student's t ‐test (a, b) or one‐way anova (c–j) was used for statistical analysis. CCK‐8, cell counting kit‐8; EdU, ethynyldeoxyuridine; ELISA, enzyme‐linked immunosorbent assay; IL, interleukin; PINK1, PTEN‐induced putative kinase 1; RT‐qPCR, reverse transcription‐polymerase chain reaction; TNF, tumor necrosis factor.

Article Snippet: TNF‐α, IL‐1β, insulin, and adiponectin concentrations in mouse serum were quantified using ELISA kits (CUSABIO) according to the manufacturer's protocol.

Techniques: Over Expression, Quantitative RT-PCR, Western Blot, CCK-8 Assay, EdU Assay, Flow Cytometry, Enzyme-linked Immunosorbent Assay, Cell Counting, Reverse Transcription, Polymerase Chain Reaction

Journal: Journal of Diabetes Investigation

Article Title: NSUN2 ‐mediated m 5 C methylation modification regulates trophoblast cell proliferation, apoptosis, and autophagy in gestational diabetes mellitus

doi: 10.1111/jdi.70140

Figure Lengend Snippet: NSUN2 inhibition alleviated inflammation and hyperglycemia in GDM pregnant mice. (a, b) Serum TNF‐α and IL‐1β levels in each group were analyzed by ELISA; (c) GTT analysis. Mice fasted for 16 h on gestation day 14–15 were subjected to GTT; (d) fasting blood glucose concentration of mice on gestation day 14–15; (e, f) serum insulin and adiponectin levels of each group mice were analyzed by ELISA. All experiments were performed with six independent biological replicates ( N = 6), each measured in triplicate. One‐way anova (a–f) was used for statistical analysis. ELISA, enzyme‐linked immunosorbent assay; GTT, glucose tolerance test; IL, interleukin; TNF, tumor necrosis factor.

Article Snippet: TNF‐α, IL‐1β, insulin, and adiponectin concentrations in mouse serum were quantified using ELISA kits (CUSABIO) according to the manufacturer's protocol.

Techniques: Inhibition, Enzyme-linked Immunosorbent Assay, Concentration Assay

Journal: Molecular Metabolism

Article Title: Deletion of PPARα in mouse brown adipocytes increases their De Novo Lipogenesis

doi: 10.1016/j.molmet.2025.102184

Figure Lengend Snippet: BAT specific deletion of PPARα does not alter glucose tolerance or body weight gain in HFD-induced obese mice. (A, H) Weight curves of control (Ctrl) and PPARαBATKO female (A) and male (H) mice ( n = 12 per group) on high fat diet (HFD) during 20 weeks. To induce CRE ERT2 activity, mice were injected intraperitoneally with tamoxifen (TAM) at a dosage of 60 mg/kg the first three days of the HFD, then every three weeks. (B, I) Glucose tolerance test (GTT) after 13 weeks of HFD in female (B) and male (I) mice, and corresponding area under curves (AUC) ( n = 8–12 per group). (C, J) Total Body weight (TBW) in female (E) and male (G) mice ( n = 4–6 per group). (D, K) Interscapular brown adipose tissue (BAT) and subcutaneous white adipose tissue (scWAT) weights in female (D) and male (K) mice ( n = 4 = 6 per group). (E, L) AT volume estimation assessed by tomography in female (E) and male (L) adult mice ( n = 3–6 per group). (F, M) Relative mRNA levels of Adiponectin and Leptin in BAT of female (F) and male (M) adult mice ( n = 4–6 per group). (G, N) Plasma levels of Adiponectin and Leptin in female (G) and male (N) mice ( n = 4–6 per group). Data are displayed as mean ± SEM. Statistical analysis was performed using 2-way ANOVA with Šídák’s post hoc test, Mann–Whitney test (E for TBW, J for Adiponectin) or student t-test for AUC. ∗ p < 0.05, vs Ctrl. £ p < 0.05, vs NaCl. NaCl: vehicle; CL: CL316,243 (β3-adrenergic agonist).

Article Snippet: Adiponectin, leptin and FGF21 levels were measured using Adiponectin (mouse) ELISA (Bertin Bioreagent, A05187 ), Leptin (mouse, rat) ELISA (Bertin Bioreagent, A05176) and Fibroblast Growth Factor 21 Mouse/Rat ELISA (Biovendor, RD291108200R) specific kits, respectively.

Techniques: Control, Activity Assay, Injection, Tomography, Clinical Proteomics, MANN-WHITNEY

Journal: Molecular Metabolism

Article Title: Deletion of PPARα in mouse brown adipocytes increases their De Novo Lipogenesis

doi: 10.1016/j.molmet.2025.102184

Figure Lengend Snippet: BAT specific deletion of PPARα induces glucose intolerance in mice fed a chow diet. (A) Experimental design. Control (UCP1-WT-PPARalphalox/lox) and PPARαBATKO (UCP1-CRE ERT2 -PPARalphalox/lox) were housed at thermoneutrality and fed a standard chow diet (CD) for 20 weeks and daily injected with 1 mg/kg of CL316,243 or NaCl the last week of the experiment. To induce CRE ERT2 activity, mice were injected intraperitoneally with tamoxifen (TAM) at a dosage of 60 mg/kg the first three days of the CD, then every three weeks. (B, K) Relative mRNA levels of Pparα in brown adipose tissue (BAT) of female (B) and male (K) adult mice ( n = 6 per group). (C, L) Relative mRNA levels of Pparα subcutaneous (scWAT) of female (C) and male (L) adult mice ( n = 6 per group). (D, M) Weight curves of control (Ctrl) and PPARαBATKO female (D) and male (M) mice ( n = 11–12 per group) on standard chow diet (CD) during 20 weeks. (F, O) Glucose tolerance test (GTT) after 13 weeks of CD in female (F) and male (O) mice, and corresponding area under curves (AUC) ( n = 12 for (F), n = 9 for (O)). (G, P) Plasma levels of Adiponectin and Leptin in female (G) and male (P) mice ( n = 4–6 per group). (H, Q) AT volume estimation assessed by tomography in female (H) and male (Q) adult mice ( n = 3–5 per group). (I, R) Subcutaneous white adipose tissue (scWAT) weights in female (I) and male (R) mice ( n = 5–6 per group). (J, S) Intrascapular brown adipose tissue (BAT) weights in female (J) and male (S) mice ( n = 5–6 per group). Data are displayed as mean ± SEM. Statistical analysis was performed using 2-way ANOVA with Šídák’s post hoc test or Mann–Whitney test (B and K). ∗ p < 0.05, vs Ctrl. £ p < 0.05, vs NaCl. Ctrl: control mice; KO: PPARαBATKO mice.

Article Snippet: Adiponectin, leptin and FGF21 levels were measured using Adiponectin (mouse) ELISA (Bertin Bioreagent, A05187 ), Leptin (mouse, rat) ELISA (Bertin Bioreagent, A05176) and Fibroblast Growth Factor 21 Mouse/Rat ELISA (Biovendor, RD291108200R) specific kits, respectively.

Techniques: Control, Injection, Activity Assay, Clinical Proteomics, Tomography, MANN-WHITNEY