copper colorimetric analysis kit  (Elabscience Biotechnology)

Journal: Current Therapeutic Research, Clinical and Experimental

Article Title: The Berberine Derivative BBR684 Inhibits VDAC Oligomerization to Suppress Ferroptosis in Acute Kidney Injury

doi: 10.1016/j.curtheres.2026.100825

Figure Lengend Snippet: BBR684 attenuates Erastin-induced ferroptosis in HK-2 cells by suppressing lipid peroxidation and activating the antioxidant response. (A) Flow cytometric analysis of lipid peroxidation using the C11-BODIPY probe in HK-2 cells treated as indicated for 12 hours. Data are presented as mean fluorescence intensity (MFI). (B) Intracellular Fe²⁺ levels measured by a ferrous iron colorimetric assay. (C, D) Levels of malondialdehyde (MDA, C) and reduced glutathione (GSH, D) in cell lysates. (E, F) Representative immunofluorescence images (E) and quantification (F) of 4-hydroxynonenal (4-HNE) adducts (red) in HK-2 cells. Nuclei were counterstained with DAPI (blue). Scale bar, 50 µm. (G) Western blot analysis of key ferroptosis-related proteins: glutathione peroxidase 4 (GPX4), heme oxygenase-1 (HO-1), and nuclear factor erythroid 2–related factor 2 (NRF2). β-actin served as the loading control. Data are from 3 independent biological replicates (n = 3) and presented as mean ± SEM. Significance was determined by one-way ANOVA followed by Tukey's HSD post hoc test. * P < 0.05, ** P < 0.01, *** P < 0.001; n.s., not significant.

Article Snippet: Intracellular Fe2+ levels were quantified using a Ferrous Iron Colorimetric Assay Kit (Catalog #E-BC-K773-M, Elabscience, Wuhan, China) per the manufacturer's protocol.

Techniques: Fluorescence, Colorimetric Assay, Immunofluorescence, Western Blot, Control

Journal: Current Therapeutic Research, Clinical and Experimental

Article Title: The Berberine Derivative BBR684 Inhibits VDAC Oligomerization to Suppress Ferroptosis in Acute Kidney Injury

doi: 10.1016/j.curtheres.2026.100825

Figure Lengend Snippet: Overexpression of VDAC abolishes the protective effects of BBR684 against ferroptosis.(A) Western blot analysis validating the overexpression of VDAC1 in HEK293T cells. (B) Representative phase-contrast microscopy images showing the morphology of HEK293T cells with or without VDAC1 overexpression after the indicated treatments for 24 hours. (C) Quantification of cell death by flow cytometry (propidium iodide staining) in HEK293T cells treated with Erastin and BBR684. (D) Cells viability assessed by the CCK-8 assay in HEK293T cells treated with increasing concentrations of BBR684 for 24 hours. (n = 3, 3 biological replicates). (E, F) Levels of malondialdehyde (MDA, F) and reduced glutathione (GSH, E) in cell lysates. (n = 3, 3 biological replicates). (G) Intracellular Fe²⁺ levels measured by a colorimetric assay. (n = 3, 3 biological replicates).

Article Snippet: Intracellular Fe2+ levels were quantified using a Ferrous Iron Colorimetric Assay Kit (Catalog #E-BC-K773-M, Elabscience, Wuhan, China) per the manufacturer's protocol.

Techniques: Over Expression, Western Blot, Microscopy, Flow Cytometry, Staining, CCK-8 Assay, Colorimetric Assay

Journal: Bioactive Materials

Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming

doi: 10.1016/j.bioactmat.2025.11.039

Figure Lengend Snippet: Continuous intraosseous administration of SCS prevents glucocorticoid-induced bone degeneration. ( A ) Schematic illustration of the glucocorticoid (GC; MPS)-induced bone deterioration and intraosseous SCS treatment. ( B-D ) Representative H&E staining images of the femur at 6 weeks (B). Magnified views of the cortical bone and trabecular bone in the marrow cavity are shown on the right. Solid arrows indicate normal osteocytes, while hollow arrows indicate empty osteocyte lacunae. Quantification of empty lacunae ratios in cortical bone (C) and trabecular bone (D). n = 6 biological replicates. (Scale bars, 500 μm and 25 μm) ( E-H ) Representative immunofluorescence staining of OPN + mature osteoblasts, osteolectin + osteoprogenitors, and VE-cadherin + endothelial cells (ECs) in femur at 6 weeks (E), and corresponding quantifications (F–H). n = 6 biological replicates. (Scale bars, 100 μm and 20 μm) ( I and J ) Representative flow cytometry plots of capillary subtypes in the femur (I), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (J). n = 6 biological replicates. ( K and L ) Flow cytometry plots showing Sca-1 hi CD31 hi arteriolar ECs (K), and corresponding quantification (L). n = 6 biological replicates. ( M and N ) Representative micro-CT 3D images of the femur (M). Quantitative analysis of percent bone volume (BV/TV) (N). n = 6 biological replicates. (Scale bars, 1.5 mm, 600 μm and 545 μm) ( O and P ) ELISA analysis of VEGF (O) and PDGF-BB (P) levels in bone marrow supernatant and peripheral serum from PBS- and SCS-treated groups at week 6. n = 6 biological replicates. ( Q ) ELISA quantification of the osteogenic factor osteocalcin in peripheral serum at week 6. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, F, G, H, J, L, N, O, P and Q ).

Article Snippet: Serum concentrations of the osteogenic marker osteocalcin (NOVUS, NBP2-68151) were also measured.

Techniques: Staining, Immunofluorescence, Flow Cytometry, Micro-CT, Enzyme-linked Immunosorbent Assay

Journal: Bioactive Materials

Article Title: Sulfated polysaccharide prevents senescent adipocyte-driven osteonecrosis by stem cell fate reprogramming

doi: 10.1016/j.bioactmat.2025.11.039

Figure Lengend Snippet: SCS targets downstream senescent lineage commitment of bone marrow MSCs to mitigate GC-induced bone deterioration. ( A ) Schematic diagram illustrating the experimental design: CD45 − Ter119 − CD31 − LepR + MSCs isolated from mice co-treated with SCS and MPS for 7 days were subjected to in vitro lineage-competitive differentiation, followed by DEX-induced senescence in lineage-mixed cells. These cells were then adoptively transplanted into healthy bone marrow cavity to assess bone deterioration development. ( B ) Representative H&E-stained images of the femur 12 weeks after adoptive transfer. PBS-DEX group: LepR + MSCs from PBS and MPS co-treated mice subjected to in vitro lineage differentiation and DEX-induced senescence, followed by transplantation. SCS-DEX group: LepR + MSCs from SCS and MPS co-treated mice processed similarly. PBS group: solvent control without cell transplantation. Solid arrows indicate intact osteocytes; hollow arrows indicate empty lacunae. (Scale bars, 250 μm and 25 μm) ( C – E ) Quantitative analysis of marrow hypertrophic adipocyte diameter (C), proportion of empty osteocyte lacunae in trabecular bone (D), and adipocyte number (E) in the metaphysis 12 weeks post-transplantation. n = 19 biological replicates (C), n = 6 biological replicates (D), n = 8 biological replicates (E). ( F ) Quantification of empty lacunae in epiphysis at 12 weeks post-transplantation. n = 6 biological replicates. ( G – I ) Representative flow cytometry plots of capillary ECs subtypes in the femur at 12 weeks (G), with quantification of CD45 − Ter119 − CD31 hi Emcn hi ECs (H) and CD45 − Ter119 − CD31 lo Emcn lo ECs (I). n = 6 biological replicates. ( J and K ) Representative flow cytometry plots (J) and corresponding quantification (K) of CD45 − Ter119 − Sca-1 hi CD31 hi arteriolar ECs in the femur at 12 weeks post-transplantation. n = 6 biological replicates. ( L ) Representative micro-CT images of the femur at 12 weeks post-transplantation across different treatment groups. (Scale bars, 1.5 mm and 500 μm) ( M – P ) Quantitative analysis of bone parameters in the metaphysis: bone mineral density (BMD) (M), percent bone volume (BV/TV) (N), trabecular separation (Tb.Sp) (O), and trabecular number (Tb.N) (P). n = 6 biological replicates. ( Q ) Serum ELISA analysis of the osteogenic marker osteocalcin at 12 weeks post-transplantation. n = 6 biological replicates. ( R and S ) ELISA analysis of PDGF-BB (R) and VEGF (S) in both bone marrow supernatant and peripheral serum at 12 weeks post-transplantation. n = 6 biological replicates. Data are presented as mean ± SD. ∗ p < 0.05, ∗∗ p < 0.01, ∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; ns, not significant. Statistical significance was determined using one-way ANOVA with Tukey's post hoc test ( C, D, E, F, H, I, K, M, N, O, P, Q, R and S ).

Article Snippet: Serum concentrations of the osteogenic marker osteocalcin (NOVUS, NBP2-68151) were also measured.

Techniques: Isolation, In Vitro, Staining, Adoptive Transfer Assay, Transplantation Assay, Solvent, Control, Flow Cytometry, Micro-CT, Enzyme-linked Immunosorbent Assay, Marker

Journal: International Journal of Pharmaceutics: X

Article Title: Ensuring vaccine cold chain integrity: A rapid and low-cost test for identifying heat-exposed sucrose-containing vaccines

doi: 10.1016/j.ijpx.2025.100467

Figure Lengend Snippet: A colorimetric glucose assay was used to measure levels of glucose in 30 μg adult and 10 μg children's COMIRNATY™ vaccines after exposure to different temperature conditions. (A) Photograph of the plate showing an increase in glucose at 37 °C and a further increase at 45 °C. The difference in colour intensity for 37 °C and 45 °C compared to 2–8 °C storage can be observed by eye without the need for a plate reader. (B) The intensity of the colour change was also analysed using a spectrophotometer at 540 nm and the concentrations of glucose in the vaccine samples were determined based on the glucose standards. The levels of glucose in temperature-altered conditions were compared to the recommended 2–8 °C storage temperature. Error bars show the standard deviations from three measurements for each temperature point. 3× FT, three freeze-thaw cycles; RT, room temperature. Ordinary one-way ANOVA with Dunnett's multiple comparisons tests. ns, not significant; ****p < 0.001.

Article Snippet: The glucose concentrations in COMIRNATYTM vaccine samples were measured using a colorimetric glucose assay kit (Cell Biolabs, San Diego, CA, USA), according to the manufacturer's protocol.

Techniques: Glucose Assay, Vaccines, Spectrophotometry

Journal: Bone Reports

Article Title: Uncoupled bone remodeling drives myeloma bone disease in Vk*MYC mouse model of multiple myeloma

doi: 10.1016/j.bonr.2026.101910

Figure Lengend Snippet: Implantation of Vk*MYC cells leads to development of MM and MMBD in recipient mice. 3D reconstruction image of femur made in Drishti Visualization Software from control (naïve) mice or mice injected with Vk*MYC cells, 8–9 weeks after inoculation. Vk*MYC mice develop lesions (black arrows) (A). Quantitation of number of lesions (B) and area of lesions (C) in mice, 8–9 weeks after intravenous injection of 250,000 Vk*MYC cells in 200 μL PBS via the tail vein. ELISA of bone turnover markers and CTX-1 (D), P1NP (E) in serum from control (naïve) mice or mice injected with Vk*MYC cells, 8–9 weeks after inoculation. Data represent mean ± S.E.M, * P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001, two tailed unpaired Student t -test.

Article Snippet: Serum concentrations of the bone formation marker amino terminal propeptide of type I procollagen (P1NP) and the bone resorption marker C-telopeptide of type I collagen (CTX-1) were determined using colorimetric ELISA kits (Immunodiagnostic Systems), following the manufacturer's instructions.

Techniques: Software, Control, Injection, Quantitation Assay, Enzyme-linked Immunosorbent Assay, Two Tailed Test