cck 8 solution  (Yeasen Biotechnology)

Journal: Bioactive Materials

Article Title: Revolutionizing Mg-based guided bone regeneration mesh derived from endogenous dentoalveolar bone augmentation

doi: 10.1016/j.bioactmat.2026.04.003

Figure Lengend Snippet: In vitro cytocompatibility assessment . (a) CCK-8 assay results of MC3T3-E1 cells and HUVECs cultured with mesh extracts. (b) Representative live/dead staining images of MC3T3-E1 cells and HUVECs after 1 and 3 days of culture. (c) Representative phalloidin (cytoskeleton) and DAPI (nucleus) staining images of MC3T3-E1 cells and HUVECs after 24 h of culture. (d) SEM images of MC3T3-E1 cells and HUVECs directly cultured on mesh surfaces for 1 day. (e) Optical images of scratch wound-healing assays for MC3T3-E1 cells cultured in different extracts for 0 h, 12 h, and 24 h. (f) Migration rates of MC3T3-E1 cells cultured in different extracts for 0 h, 12 h, and 24 h. n.s.>0.05, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001.

Article Snippet: On days 1, 3, and 5 of culture, the existing culture medium was substituted with 100 μL of CCK-8 working solution (Cell Counting Kit-8, Beyotime Biotech, China), prepared by mixing fresh α-MEM and CCK-8 reagent at a volume ratio of 10:1.

Techniques: In Vitro, CCK-8 Assay, Cell Culture, Staining, Migration

Journal: Frontiers in Neurology

Article Title: Salvianolic acid B alleviates depression-like behaviors by reducing neuronal injury and promoting neurogenesis in a manner associated with JAK-STAT signaling pathway inhibition

doi: 10.3389/fneur.2026.1817261

Figure Lengend Snippet: SalB attenuated CORT-induced HT22 cell damage. (A) HT22 cells were exposed to 0–250 μM CORT for 24 h, and CCK-8 assessed cell viability. (B) HT22 cells were treated with 2.5–40 μM SalB for 24 h, and CCK-8 assessed cell viability. (C) HT22 cells were pretreated with 10, 15 and 20 μM SalB for 1 h, and then stimulated with 200 μM CORT for 24 h. CCK-8 assessed cell viability. SalB significantly increased it. (D) The LDH level of the cells was detected by the kit, which was significantly reduced after SalB intervention. (E, F) Flow cytometry detected apoptosis level, which was significantly reduced after SalB intervention. (G–I) ELISA detected inflammatory factor content. SalB markedly declined TNF-α, IL-1β and IL-6 contents. (J, K) The intracellular ROS level was assessed using flow cytometry, which was markedly lessened after SalB intervention. (L–N) Oxidative stress indexes were detected by kits. SalB significantly increased GSH-Px and SOD activities and decreased MDA contents. n = 3, ** p < 0.01, *** p < 0.001 vs. 0/Control group; # p < 0.05, ## p < 0.01, ### p < 0.001 vs. CORT group.

Article Snippet: Subsequently, 10 μl of cell counting kit (CCK)-8 solution (G4103, Servicebio, Wuhan, China) was added and incubated for 2 h. The optical density (OD) at 450 nm was detected by a microplate reader (1410101, ThermoFisher Scientific, Waltham, MA, USA), and the cell viability was calculated to determine the optimal administration conditions.

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

Journal: Frontiers in Neurology

Article Title: Salvianolic acid B alleviates depression-like behaviors by reducing neuronal injury and promoting neurogenesis in a manner associated with JAK-STAT signaling pathway inhibition

doi: 10.3389/fneur.2026.1817261

Figure Lengend Snippet: SalB attenuated CORT-induced HT-22 cell injury by JAK-STAT signaling. (A) CCK-8 detected cell viability. RO8191 significantly reduced cell viability. (B) The LDH level of cells was detected by the kit, which was significantly increased after RO8191 intervention. (C, D) Flow cytometry detected apoptosis level, which was significantly increased after RO8191 intervention. (E–G) ELISA detected inflammatory factor content. RO8191 markedly enhanced TNF-α, IL-1β and IL-6 contents. (H–J) Oxidative stress index was detected by kit. RO8191 significantly reduced GSH-Px and SOD activities and increased MDA contents. (K, L) The intracellular ROS level was detected by flow cytometry, which was significantly increased after RO8191 intervention. n = 3, *** p < 0.001 vs. Control group; ## p < 0.01, ### p < 0.001 vs. CORT group; & p < 0.05, && p < 0.01 vs. CORT+20 μM SalB group.

Article Snippet: Subsequently, 10 μl of cell counting kit (CCK)-8 solution (G4103, Servicebio, Wuhan, China) was added and incubated for 2 h. The optical density (OD) at 450 nm was detected by a microplate reader (1410101, ThermoFisher Scientific, Waltham, MA, USA), and the cell viability was calculated to determine the optimal administration conditions.

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

Journal: Oncology Letters

Article Title: Exosomal-miR-32-5p directly targets FOXN2 to regulate the proliferation, migration and apoptosis of uterine corpus endometrial carcinoma via the PI3K/AKT/BCL-2 pathway

doi: 10.3892/ol.2026.15574

Figure Lengend Snippet: Effects of miR-32-5p on the proliferative capacities, migratory abilities and apoptotic rate of UCEC cells. (A) The expression of miR-32-5p in HEC-1-A and Ishikawa cells were then determined using quantitative reverse transcription-PCR. ***P<0.001 vs. HEC-1-A cells. (B) The expression of miR-32-5p in HEC-1-A cells after transfection of miR-32-5p inhibitor or in Ishikawa cells after transfection of miR-32-5p mimic. (C) The viability of UCEC cell lines were measured using the CCK-8 assay. (D) Relative colony formation efficiency of UCEC cell lines was evaluated using the colony formation assay. (E) EdU-positive cells were measured through EdU proliferation assay. (Scale bar, 100 µm). (F) The migratory potential of UCEC cell lines were determined via Transwell migration assay. (Scale bar, 100 µm). (G) Flow cytometry was used to detect apoptosis. * P<0.05, **P<0.01, ***P<0.001 vs. miR-32-5p inhibitor-NC or miR-32-5p mimic-NC. UCEC, uterine corpus endometrial carcinoma; miRNA, microRNA; NC, negative control; EdU, 5-ethynyl-2′-deoxyuridine.

Article Snippet: HEC-1-A or Ishikawa cells (3×10 3 cells/ml) were grown in 96-well plates for 0, 24, 48 and 72 h before adding the CCK-8 solution (15 μl; Dojindo Laboratories, Inc.).

Techniques: Expressing, Reverse Transcription, Transfection, CCK-8 Assay, Colony Assay, Proliferation Assay, Transwell Migration Assay, Flow Cytometry, Negative Control

Journal: Oncology Letters

Article Title: Exosomal-miR-32-5p directly targets FOXN2 to regulate the proliferation, migration and apoptosis of uterine corpus endometrial carcinoma via the PI3K/AKT/BCL-2 pathway

doi: 10.3892/ol.2026.15574

Figure Lengend Snippet: Exo-miR-32-5p regulates the proliferation, migration and apoptosis of UCEC cells through regulating FOXN2 expression and PI3K/AKT/Bcl-2 pathway. The impact of Exo-miR-32-5p on the proliferation, migration and apoptosis of UCEC cells were examined utilizing a co-culture model. (A) Exo-miR-32-5p expression in HEC-1-A cells transfected with miR-32-5p-inhibitor or in Ishikawa cells transfected with miR-32-5p-mimic was determined through qRT-PCR. (B) The viability of UCEC cell lines were measured using the CCK-8 assay. (C) Relative colony formation efficiency of UCEC cell lines was evaluated using the colony formation assay. (D) EdU-positive cells were measured through EdU proliferation assay. (Scale bar, 100 µm). (E) The migratory potential of UCEC cell lines were determined via the Transwell migration assay. (F) Flow cytometry was used to detect apoptosis. (G) The mRNA expression of AKT, PI3K, Bcl-2 and FOXN2 was detected by qRT-PCR. (H) The protein levels of AKT, PI3K, p-PI3K, Bcl-2, FOXN2 and the ratio of p-AKT/AKT were measured by western blotting. **P<0.01, ***P<0.001 vs. Exo-miR-32-5p inhibitor-NC or Exo-miR-32-5p mimic-NC. UCEC, uterine corpus endometrial carcinoma; miRNA, microRNA; NC, negative control; NS, not significant; WT, wild-type; MUT, mutant; qRT-PCR, quantitative reverse transcription-PCR; p-, phosphorylated; FOXN2, Forkhead Box N2; EdU, 5-ethynyl-2′-deoxyuridine.

Article Snippet: HEC-1-A or Ishikawa cells (3×10 3 cells/ml) were grown in 96-well plates for 0, 24, 48 and 72 h before adding the CCK-8 solution (15 μl; Dojindo Laboratories, Inc.).

Techniques: Migration, Expressing, Co-Culture Assay, Transfection, Quantitative RT-PCR, CCK-8 Assay, Colony Assay, Proliferation Assay, Transwell Migration Assay, Flow Cytometry, Western Blot, Negative Control, Mutagenesis, Reverse Transcription