ldh assay kit  (Dojindo Labs)

Journal: Journal of Cellular and Molecular Medicine

Article Title: TARDBP Mediates the MAP 3 K 11/ SLC 3 A 2/ GPX 4 Axis in Alzheimer's Disease Rats by Enhancing KRAS m RNA Stability

doi: 10.1111/jcmm.71181

Figure Lengend Snippet: Fer‐1 inhibits Aβ 1–42 ‐induced PC12 cell injury, ROS production and iron accumulation. (A) Cell viability detected by MTT; (B) LDH content detected by LDH assay kit; (C) Intracellular ROS assay; (D) Fe 2+ concentration assay; (E, F) Levels of MDA and 4‐HNE were measured using commercial kits. Data are expressed as mean ± standard deviation. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: LDH levels were measured using the LDH assay kit (CK12, Dojindo, Japan).

Techniques: Lactate Dehydrogenase Assay, ROS Assay, Concentration Assay, Standard Deviation

Journal: Journal of Cellular and Molecular Medicine

Article Title: TARDBP Mediates the MAP 3 K 11/ SLC 3 A 2/ GPX 4 Axis in Alzheimer's Disease Rats by Enhancing KRAS m RNA Stability

doi: 10.1111/jcmm.71181

Figure Lengend Snippet: Up‐regulation of KRAS attenuates the ameliorative effect of down‐regulation of TARDBP on Aβ 1–42 ‐induced PC12 cells. (A) RT‐qPCR to verify successful transfection; (B) MTT to detect cell viability; (C) LDH assay kit to detect LDH content; (D) Intracellular ROS assay; (E) Fe 2+ concentration assay; (F, G) Levels of MDA and 4‐HNE were measured using commercial kits. Data are expressed as mean ± standard deviation. * p < 0.05, ** p < 0.01, *** p < 0.001, **** p < 0.0001.

Article Snippet: LDH levels were measured using the LDH assay kit (CK12, Dojindo, Japan).

Techniques: Quantitative RT-PCR, Transfection, Lactate Dehydrogenase Assay, ROS Assay, Concentration Assay, Standard Deviation

Journal: bioRxiv

Article Title: Lipid A counteracts doxorubicin-induced systemic dysfunction by boosting mitochondrial activity

doi: 10.64898/2026.04.16.719094

Figure Lengend Snippet: (A, B) LVEF (A) and LVFS (B) 4 weeks after adjuvant administration. (C, D) Body weight (C) and heart weight (D) 4 weeks after adjuvant administration (n = 4-6 mice per group). (E, F) Cytotoxicity in NRCMs 20 hours after adjuvant treatment. Cell viability and toxicity were measured by LDH release and MTT assay (n = 3). All data are shown as mean ± SEM; Data were analyzed using one-way ANOVA followed by Tukey’s comparison test.

Article Snippet: Twenty hours after drug treatment, cytotoxicity and cell viability were evaluated using the Cytotoxicity LDH Assay Kit-WST (Dojindo Molecular Technologies, Inc., Kumamoto, Japan) and the Cell Counting Kit-8 (Dojindo Molecular Technologies, Inc., Kumamoto, Japan), respectively, in accordance with the manufacturers’ manuals.

Techniques: Adjuvant, MTT Assay, Comparison

Journal: Cell Reports Medicine

Article Title: Engineered oncolytic virus armed with anti-PCSK9 scFv boosts long-term CD8 + T cell immunity via rewiring MHC-I antigen presentation

doi: 10.1016/j.xcrm.2026.102724

Figure Lengend Snippet: OVs impaired CD8 + T cell response via inducing MHC-I degradation (A) C57 mice with MC38 subcutaneous xenografts were treated with VSVΔ51 (2 × 10 7 plaque-forming unit (PFU)/day, i.t., intra-tumoral injection). The CD45 + cells were isolated from MC38 tumor at 16 days for scRNA-seq analysis ( GSE293436 ). (B) UMAP plot of the 10 major cell types in MC38 tumor-bearing mice. (C) KEGG analysis demonstrates the changed signaling in T cell cluster following VSVΔ51 treatment. (D and E) LDH release assay was performed to detect the cytotoxicity of T lymphocytes. CT26-OVA cells were co-cultured with the OT1 T cells at indicated ratio (E:T = 1:1, 1:5, or 1:10) in the CM-Uninfected, CM-VSVΔ51-UV(D), or CM-VSVΔ51ΔG (E) for 24 h. (F and G) Flow cytometry analysis and quantification of cell surface MHC-I expression. CT26 cells were treated with CM-Uninfected, CM-VSVΔ51-UV (F), or CM-VSVΔ51ΔG (G) for 24 h. Then the expression of MHC-I was measured by flow cytometry. (H) DLD1 and HCT116 were infected with escalating titers of VSVΔ51 for 24 h. Or DLD1 and HCT116 were infected with VSVΔ51, MOI = 0.05, for different times. Flow cytometry plots and quantification of cell-surface MHC-I. Statistical significance was determined using two-tailed unpaired Student’s t test in (D, E, F, and G) and one-way ANOVA in (H). Data represent the mean ± SD. n = 3 biological replicates in (D, E, F, G, and H). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ns, nonsignificant.

Article Snippet: Cytotoxicity LDH Assay Kit , DOJINDO , Cat# CK12-2000T.

Techniques: Injection, Isolation, Lactate Dehydrogenase Assay, Cell Culture, Flow Cytometry, Expressing, Infection, Two Tailed Test

Journal: Cell Reports Medicine

Article Title: Engineered oncolytic virus armed with anti-PCSK9 scFv boosts long-term CD8 + T cell immunity via rewiring MHC-I antigen presentation

doi: 10.1016/j.xcrm.2026.102724

Figure Lengend Snippet: The combination of VSVΔ51 and PCSK9 inhibition fosters the stem-like CD8 + T cells and established the anti-tumor memory (A and B) Immune cell depletion experiments. BALB/c mice were injected with anti-mouse CD8, anti-mouse CD4, or isotype antibody for 5 doses (10 mg/kg). Validation of immune cell depletion (A). CT26-bearing mice were subjected to immune cell depletion and then received the combination treatment of alirocumab (10 mg/kg/day, intraperitoneal injection) and VSVΔ51 (3 × 10 7 PFU/day, intravenous injection). Tumor volumes of the mice were recorded ( n = 3) (B). (C and D) CT26 subcutaneous tumor model. The representative image of CD4 + and CD8 + T cells were analyzed in subcutaneous xenograft tumor tissue by flow cytometry. The activity of CD8 + T cells was evaluated by measuring GranzB and IFN-γ expression (C). Quantification and functional activity analysis of tumor-infiltrating lymphocyte in CT26 tumor (D). (E) Tumor-free mice from the CT26 model, which had been treated with a combination of VSVΔ51 and PCSK9i, were rechallenged on day 50. They received a 2-fold increase in the number of homogeneous CT26 cells (4 × 10 6 ) in the right side of mice and heterogeneous 4T1 cells (1 × 10 6 ) in left side of mice. Naive mice of similar age (3 months) were implanted with the same tumor cells as controls ( n = 3). (F and G) The homogeneous CT26 and 4T1 tumor volume (F) and tumor burden (G) were recorded in the experiment (E). (H) Flow cytometry analysis of the percentages and function of the T cells from naive mice and cured mice from CT26 tumor in the spleen. (I and J) The in vitro analysis of the anti-tumor memory of T lymphocytes from the spleen. T lymphocytes were obtained from the spleen of naive or tumor-free mice ( n = 3) by magnetic beads and co-cultured with CT26 and 4T1, respectively. LDH release assays were performed to measure the tumor-specific cytotoxicity when co-cultured with CT26 and 4T1 tumor cells (I). The activity of T cells was evaluated by measuring CD107A and Ki-67 expression. The representative images of flow cytometry analysis were presented. The ratio of CD107A + CD8 + T, Ki-67 + CD4 + T, and Ki-67 + CD8 + T were quantified (J). Statistical significance was determined using one-way ANOVA in (D, H, and L) and two-way ANOVA in (B, F, and J). Data represent the mean ± SD. n = 2 biological replicates in (P, Q, R, and S). n = 5 biological replicates in (B, C, D, F, G, H, J, K, and L). ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ns, nonsignificant.

Article Snippet: Cytotoxicity LDH Assay Kit , DOJINDO , Cat# CK12-2000T.

Techniques: Inhibition, Injection, Biomarker Discovery, Flow Cytometry, Activity Assay, Expressing, Functional Assay, In Vitro, Magnetic Beads, Cell Culture