Journal: Oncology Reports

Article Title: Knockdown of CCT2 inhibits the malignant progression of hepatocellular carcinoma cells by impairing STAT3 activation

doi: 10.3892/or.2026.9086

Figure Lengend Snippet: IL-6 abolishes the effects of CCT2 knockdown on the proliferation and invasion of hepatocellular carcinoma cells. The protein levels of STAT3 and p-STAT3 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The proliferation of (C) Huh-7 and (D) HCCLM3 cells following CCT2 knockdown and IL-6 treatment was detected using EdU incorporation assay. The invasion of (E) Huh-7 and (F) HCCLM3 cells was assessed using Transwell assay. *P<0.05, **P<0.01 vs. PBS. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; p-, phosphorylated.

Article Snippet: Recombinant human IL-6 (cat. no. HY-P7044; MedChemExpress) as used for STAT3 activation.

Techniques: Knockdown, Western Blot, Transwell Assay

Journal: Bioactive Materials

Article Title: Bioengineered extracellular vesicles escape lysosomal degradation and deliver Tet-PKM2 for macrophage immunometabolic reprogramming and periodontitis treatment

doi: 10.1016/j.bioactmat.2026.01.002

Figure Lengend Snippet: Immunomodulatory effects of the bioengineered LEVs Tet−PKM2 @TA in terms of their ability to modulate macrophage polarization in vitro . The macrophages were treated with 100 ng/mL LPS for 24 h and then treated with PBS (Control), 100 μg/mL LEVs PKM2 , LEVs Tet−PKM2 , or LEVs Tet−PKM2 @TA for another 24 h. ( A ) The relative mRNA expression levels of M1 polarization-related genes ( IL-6 and IL-1β ) and M2 polarization-related genes ( IL-4 and Arg-1 ) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (qRT‒PCR) ( n = 3). ( B ) Concentrations of M1-related cytokines (IL-6 and TNF-α) and M2-related cytokines (IL-4 and IL-10) in the supernatants of the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups (ELISA) ( n = 3). ( C ) Representative immunofluorescence images and quantification of the expression levels of M1-related proteins (iNOS and CCR7) and M2-related proteins (CD163, CD206, and Arg-1) in the Control, LEVs PKM2 , LEVs Tet−PKM2 , and LEVs Tet−PKM2 @TA groups ( n = 3). The data are expressed as the mean ± SEM. Statistical analysis was performed with one-way ANOVA ( A , B , and C ). ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001 indicate significant differences between the indicated columns.

Article Snippet: Kits were sourced as follows: TNF-α, IL-4, and IL-10 from Fankew (Shanghai Kexing Trading Co., Ltd., China) and IL-6 from Proteintech.

Techniques: In Vitro, Control, Expressing, Enzyme-linked Immunosorbent Assay, Immunofluorescence

Journal: International Journal of Molecular Medicine

Article Title: DUSP26: Unveiling a critical molecular mediator and therapeutic target in developmental dysplasia of the hip-associated secondary osteoarthritis

doi: 10.3892/ijmm.2026.5776

Figure Lengend Snippet: Significant Ups genes in the acetabular cartilage of the rats with DDH, as determined by mRNA-seq analysis. (A) Neonatal rats were subjected to straight-leg swaddling for 10 days. A total of 4 weeks later, (a) morphology, (b) H&E staining and (c) SO/FG staining were assessed in the hip joints of the rats. (B) Immunohistochemical staining and (E) semi-quantitative analysis of COL2A1 in the acetabular cartilage of the 4-week-old control rats and rats with DDH. (C) Relative gene expression levels of COL2A1, IL-1β and IL-6 in the acetabular cartilage of the 4-week-old control rats and rats with DDH, as determined by reverse transcription-quantitative PCR. (D) Levels of IL-6 in the supernatants of acetabular cartilage from the 4-week-old rats with DDH, as determined by ELISA. (F) Significant Ups in the acetabular cartilage of rats with DDH were identified by mRNA-seq analysis with the screening criteria of log 2 FC >4 and P.adj<0.01. Principal component analysis results and a heatmap of these significant Ups are shown. (G) GO enrichment analysis of significant Ups in the acetabular cartilage of the rats with DDH. Data are presented as the mean ± SD. *** P<0.001. (C-E) Representative results of four independent experiments are shown. Ups, upregulated genes; BP, biological process; CC, cellular component; COL2A1, type II collagen; DDH, developmental dysplasia of the hip; FC, fold change; GO, Gene Ontology; H&E, hematoxylin and eosin; IHC, immunohistochemistry; IL, interleukin; IOD, integrated optical density; MF, molecular function; mRNA-seq, mRNA sequencing; SO/FG, Safranin O/Fast Green.

Article Snippet: Protein concentrations were measured using a BCA assay kit (cat. no. PK10026; Wuhan Sanying Biotechnology), and the levels of TNF-α and IL-6 in the tissue homogenates and cell supernatants were measured using the Rat TNF-α ELISA Kit (cat. no. EK382; Multi Sciences Biotech) and Rat IL-6 ELISA Kit (cat. no. EK306; Multi Sciences Biotech), according to the manufacturers' instructions.

Techniques: Staining, Immunohistochemical staining, Control, Gene Expression, Reverse Transcription, Real-time Polymerase Chain Reaction, Enzyme-linked Immunosorbent Assay, Immunohistochemistry, Sequencing

Journal: International Journal of Molecular Medicine

Article Title: DUSP26: Unveiling a critical molecular mediator and therapeutic target in developmental dysplasia of the hip-associated secondary osteoarthritis

doi: 10.3892/ijmm.2026.5776

Figure Lengend Snippet: DUSP26 overexpression alleviates IL-1β-induced chondrocyte injury. Rat DUSP26 overexpression adenovirus was constructed and used to infect chondrocytes. After 24 h, the chondrocytes were subjected to 10 ng/ml IL-1β. (A) Expression levels of COL2A1 and COL1A1 in the chondrocytes were detected by RT-qPCR and western blotting. (B) Relative mRNA expression levels of TNF-α and IL-6 in the chondrocytes were determined by RT-qPCR. (C) Levels of TNF-α and IL-6 in the supernatants of the chondrocytes were determined by ELISA. Two adenovirus-mediated shRNAs against rat DUSP26 were constructed and used to infect chondrocytes. After 24 h, the chondrocytes were subjected to 10 ng/ml IL-1β. (D) Expression levels of COL2A1 and COL1A1 in the chondrocytes were evaluated by RT-qPCR and western blotting. (E) Relative mRNA expression levels of TNF-α and IL-6 in the chondrocytes were determined by RT-qPCR. (F) Levels of TNF-α and IL-6 in the supernatants of the chondrocytes were detected by ELISA. Data are presented as the mean ± SD. * P<0.05, ** P<0.01 and *** P<0.001. Representative results of three independent experiments are shown. COL1A1, type I collagen; COL2A1, type II collagen; EP, empty adenoviral vector; DUSP26, dual-specificity phosphatase 26; IL, interleukin; NC, negative control; RT-qPCR, reverse transcription-quantitative PCR; sh, short hairpin.

Article Snippet: Protein concentrations were measured using a BCA assay kit (cat. no. PK10026; Wuhan Sanying Biotechnology), and the levels of TNF-α and IL-6 in the tissue homogenates and cell supernatants were measured using the Rat TNF-α ELISA Kit (cat. no. EK382; Multi Sciences Biotech) and Rat IL-6 ELISA Kit (cat. no. EK306; Multi Sciences Biotech), according to the manufacturers' instructions.

Techniques: Over Expression, Construct, Expressing, Quantitative RT-PCR, Western Blot, Enzyme-linked Immunosorbent Assay, Plasmid Preparation, Negative Control, Reverse Transcription, Real-time Polymerase Chain Reaction

Journal: Materials Today Bio

Article Title: One-step green assembly of natural polyphenol-based nobiletin nanoparticles for ulcerative colitis therapy

doi: 10.1016/j.mtbio.2026.102887

Figure Lengend Snippet: | In vivo anti-oxidant and anti-inflammatory effects of NTAl NPs against UC. A) H&E-stained sections of mouse colon following treatment with indicated materials. B) H&E staining histological scores. C) Typical TEM images showing the microstructures of colonic epitheliums. D-F) the expression of oxidative stress markers including MDA(D), SOD (E), and GSH-Px (F). G-J) the expression of colonic inflammatory cytokines including pro-inflammatory cytokines TNF-α (G), IL-1β (H), IL-6 (I) and anti-inflammatory cytokines IL-10 (J). All data are shown as mean ± s.d; n = 6. ∗ P < 0.05, ∗∗ P < 0.01, ∗∗∗ P < 0.001.

Article Snippet: Commercial ELISA kits including Mouse TNF-α (EK282, Multi Sciences), Mouse IL-1β (EK201B, Multi Sciences), Mouse IL-6 (EK206, Multi Sciences), and Mouse IL-10 (EK210, Multi Sciences) were used to quantify pro-inflammatory cytokines and the anti-inflammatory cytokine according to the manufacturer's instructions.

Techniques: In Vivo, Staining, Expressing

Journal: Hepatology Communications

Article Title: B4GALT1 deficiency attenuates steatohepatitis by regulating the PPARγ/ACSL4 axis

doi: 10.1097/HC9.0000000000000920

Figure Lengend Snippet: Hepatic loss of B4galt1 alleviates fatty degeneration and inflammation in MASLD mice. (A) Schematic diagram of a murine model fed a chow diet or CDAHFD. (B) Body weight (n=8–10/group) and liver weight/body weight (%) (n=6–8/group) were measured in B4galt1 flox/flox and B4galt1 hep−/− mice fed a chow diet or CDAHFD. (C) Serum levels of ALT and AST were measured (n=6–8/group). (D) Levels of TNF-α and IL-6 in the liver tissues were detected using ELISA (n=6–8/group). (E) Serum and hepatic levels of TG, TC, LDL, and NEFA were tested (n=5–8/group). (F) Sections of paraffin-embedded liver tissue were subjected to H&E, Sirius red staining, and immunohistochemical staining for α-SMA and F4/80. Frozen sections were stained with Oil Red O. Scale bars, 100 µm. (G) Steatosis, lobular inflammation scores, and total NAS for each group (n=8–10/group). (H) Quantification of Oil Red O, F4/80, and Sirius red staining. Data are presented as mean ± SEM (* p <0.05, ** p <0.01, *** p <0.001, **** p <0.0001; ANOVA). Abbreviations: B4GALT1, β-1,4-galactosyltransferase 1; CDAHFD, choline-deficient, L–amino acid–defined, high-fat diet; ELISA, enzyme-linked immunosorbent assay; H&E, hematoxylin and eosin; MASLD, metabolic dysfunction–associated steatotic liver disease; NAS, NAFLD activity score.

Article Snippet: Plasma TNF-α (EK282; Multi Sciences Biotech) and IL-6 (EK206; Multi Sciences Biotech) concentrations were quantified using mouse enzyme-linked immunosorbent assay (ELISA) kits according to the manufacturer’s instructions.

Techniques: Enzyme-linked Immunosorbent Assay, Staining, Immunohistochemical staining, Activity Assay