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: Knockdown of CCT2 inhibits STAT3 signaling activation in hepatocellular carcinoma cells. The protein levels of STAT3, p-STAT3, MCL1, MMP2 and SOX2 in (A) Huh-7 and (B) HCCLM3 cells were measured by western blotting. The protein levels of (C) p-STAT3, (D) MCL1, (E) MMP2 and (F) SOX2 in subcutaneous tumor tissue were detected by immunohistochemical staining. *P<0.05, **P<0.01 vs. sh-NC. CCT2, chaperonin containing TCP1 subunit 2; sh, short hairpin; NC, negative control; p, phosphorylated; MCL1, myeloid cell leukemia sequence 1; SOX2, SRY-box transcription factor 2.

Article Snippet: The primary antibodies were as follows: CCT2 (cat. no. 24896-1-AP), β-actin (cat. no. 66009-1-Ig), MMP2 (cat. no. 10373-2-AP), myeloid cell leukemia sequence 1 (MCL1; cat. no. 16225-1-AP) and SRY-box transcription factor 2 (SOX2; cat. no. 11064-1-AP; all Proteintech Group, Inc.) and STAT3 (cat. no. 4904) and phosphorylated (p-)STAT3 (Tyr705; cat. no. 4113; both Cell Signaling Technology, Inc.) The membranes were washed three times in TBST (0.1% Tween-20) for 5 min each at room temperature.

Techniques: Knockdown, Activation Assay, Western Blot, Immunohistochemical staining, Staining, Negative Control, Sequencing

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: The primary antibodies were as follows: CCT2 (cat. no. 24896-1-AP), β-actin (cat. no. 66009-1-Ig), MMP2 (cat. no. 10373-2-AP), myeloid cell leukemia sequence 1 (MCL1; cat. no. 16225-1-AP) and SRY-box transcription factor 2 (SOX2; cat. no. 11064-1-AP; all Proteintech Group, Inc.) and STAT3 (cat. no. 4904) and phosphorylated (p-)STAT3 (Tyr705; cat. no. 4113; both Cell Signaling Technology, Inc.) The membranes were washed three times in TBST (0.1% Tween-20) for 5 min each at room temperature.

Techniques: Knockdown, Western Blot, Transwell Assay

Journal: Frontiers in Aging Neuroscience

Article Title: Unraveling the anti-neuroinflammatory mechanisms of Cervus cucumis polypeptide injection in Alzheimer’s disease: insights from network pharmacology, molecular docking, molecular dynamics simulation, and experimental validation

doi: 10.3389/fnagi.2026.1797302

Figure Lengend Snippet: Effects of CCPI on the expression of IL-6/STAT3/VEGF signaling pathway. (A) Western blot showed the expression of the IL-6/STAT3/VEGF pathway after CCPI treatment. (B–D) Quantitative analysis of the IL-6/GAPDH, STAT3/GAPDH, and VEGF/GAPDH ratios in the CCPI-treated groups, respectively. Data are presented as mean ± SD ( n = 3). ### p < 0.001 vs. ontrol group; *** p < 0.001, ** p < 0.01 and * p < 0.05 vs. AD model group.

Article Snippet: After being blocked in 5% skim milk for 2 h at room temperature, the membranes were incubated overnight with the following primary antibodies: inducible nitric oxide synthase (iNOS) mouse antibody (CAS No. IC259554, Abmart, China, 1:1,000), CD206 mouse antibody (CAS No. ZY-5843R, Abmart, China, 1:1,000), IL-6 mouse antibody (CAS No. 66146-2, Abmart, China, 1:1,000), STAT3 mouse antibody (CAS No. YA056, Abmart, China, 1:1,000), STAT3 phosphorylation mouse antibody (CAS No. 05-485, Sigma, United States, 1:1,000), VEGF rabbit antibody (CAS No. AF1309, Abmart, China, 1:1,000) and GAPDH rabbit antibody (CAS No. 10494-1-AP, Abmart, China, 1:1,000).

Techniques: Expressing, Western Blot

Journal: Frontiers in Aging Neuroscience

Article Title: Unraveling the anti-neuroinflammatory mechanisms of Cervus cucumis polypeptide injection in Alzheimer’s disease: insights from network pharmacology, molecular docking, molecular dynamics simulation, and experimental validation

doi: 10.3389/fnagi.2026.1797302

Figure Lengend Snippet: Comparison of the effects of CCPI and LA on IL-6 secretion, STAT3 phosphorylation, and the expression of markers associated with pro-inflammation (iNOS) and anti-inflammation/repair (CD206) in AD model cells. (A) IL-6 levels in the AD model cells were measured by ELISA. (B) Western blot showed the expression of iNOS, CD206, STAT3 phosphorylation, and STAT3 after CCPI and LA treatment. (C–E) Quantitative analysis of the iNOS/GAPDH, CD206/GAPDH, and STAT3 phosphorylation/STAT3 ratios in the CCPI and LA-treated groups, respectively. Data are presented as mean ± SD ( n = 3). ### p < 0.001 vs. control group; *** p < 0.001, ** p < 0.01 and * p < 0.05 vs. AD model group; ns p > 0.05 compared with the CCPI group; compared with the LA group, ns p > 0.05.

Article Snippet: After being blocked in 5% skim milk for 2 h at room temperature, the membranes were incubated overnight with the following primary antibodies: inducible nitric oxide synthase (iNOS) mouse antibody (CAS No. IC259554, Abmart, China, 1:1,000), CD206 mouse antibody (CAS No. ZY-5843R, Abmart, China, 1:1,000), IL-6 mouse antibody (CAS No. 66146-2, Abmart, China, 1:1,000), STAT3 mouse antibody (CAS No. YA056, Abmart, China, 1:1,000), STAT3 phosphorylation mouse antibody (CAS No. 05-485, Sigma, United States, 1:1,000), VEGF rabbit antibody (CAS No. AF1309, Abmart, China, 1:1,000) and GAPDH rabbit antibody (CAS No. 10494-1-AP, Abmart, China, 1:1,000).

Techniques: Comparison, Phospho-proteomics, Expressing, Enzyme-linked Immunosorbent Assay, Western Blot, Control

Journal: Scientific Reports

Article Title: Adapalene, an RAR agonist, exerts anti-inflammatory effects by regulating macrophage polarization through RAR -mediated signaling pathways

doi: 10.1038/s41598-026-44454-z

Figure Lengend Snippet: Adapalene reduces LPS-stimulated MAPK and PI3K/Akt signaling in murine macrophages. RAW264.7 cells were pretreated with or without adapalene (10, 100, or 1000 nM) for 1 h and then stimulated with LPS (100 ng/mL) for 30 min. Total cellular proteins were resolved using SDS-PAGE and detected using specific antibodies against p-p38, p38, p-JNK, JNK, p-ERK, ERK (A), p-Akt, Akt, p-PI3K, PI3K, p-STAT3, and STAT3 (B). β-actin was used as an internal control. Membranes were cut prior to antibody incubation; all available uncropped images are provided in the Supplementary Information. Original full-length images for certain replicates are unavailable due to loss of original acquisition files. Representative results are shown and density analysis is presented as the mean ± S.D. of three independent experiments in lower panel. AD; adapalene, * P < 0.05, ** P < 0.01, and *** P < 0.001 vs. control; # P < 0.05 and ## P < 0.01 vs. LPS alone.

Article Snippet: t-STAT3 , Cell Signaling , 9139 , Mouse , 1:1000.

Techniques: SDS Page, Control, Incubation

Journal: Scientific Reports

Article Title: Adapalene, an RAR agonist, exerts anti-inflammatory effects by regulating macrophage polarization through RAR -mediated signaling pathways

doi: 10.1038/s41598-026-44454-z

Figure Lengend Snippet: RARβ mediates adapalene-induced anti-inflammatory signaling. (A, B) RAW264.7 cells were transfected with control siRNA or RARβ siRNA (100 nM), and then treated with LPS in the presence or absence of adapalene for 24 h. Total cellular proteins were resolved using SDS-PAGE and detected using the specific antibodies p-p38, p38, p-JNK, JNK, p-ERK, and ERK (A) and specific antibodies p-Akt, Akt, p-PI3K, PI3K, p-STAT3, and STAT3 (B). (C, D) RAW264.7 cells were treated in the presence or absence of LE135 (0.1–10 µM) with or without adapalene and LPS for 24 h. Total cellular proteins were resolved using SDS-PAGE and detected using specific antibodies p-p38, p38, p-JNK, JNK, p-ERK, and ERK (C) and specific antibodies p-Akt, Akt, p-PI3K, PI3K, p-STAT3, and STAT3 (D). Membranes were cut prior to antibody incubation; all available uncropped images are provided in the Supplementary Information. Original full-length images for certain replicates are unavailable due to loss of original acquisition files. Density analyses are shown in lower panel. The experiment was performed three times in triplicate and results are presented as the mean ± S.D. of three independent experiments. AD; adapalene, * P < 0.05, ** P < 0.01, and *** P < 0.001 vs. control; # P < 0.05, ## P < 0.01, and ### P < 0.001 vs. LPS alone; & P < 0.05, && P < 0.01, and &&& P < 0.001 vs. AD plus LPS.

Article Snippet: t-STAT3 , Cell Signaling , 9139 , Mouse , 1:1000.

Techniques: Transfection, Control, SDS Page, Incubation

Journal: Scientific Reports

Article Title: Adapalene, an RAR agonist, exerts anti-inflammatory effects by regulating macrophage polarization through RAR -mediated signaling pathways

doi: 10.1038/s41598-026-44454-z

Figure Lengend Snippet: In vivo anti-inflammatory effects of adapalene in LPS-induced septic shock model. Six mice per group were treated with vehicle only or adapalene (20, 50, or 100 mg/kg, p.o. ) for 1 h and then injected with LPS (25 mg/kg, i.p. ). Serum and liver samples were collected from each mouse after 6 h. (A, B) TNFα, IL-6, and IL-1β protein in serum (A) and mRNA levels of TNFα, IL-1β, IL-6, iNOS, and COX-2 in liver (B) were determined using EIA and qRT-PCR, respectively. (C) TNFα, IL-1β, IL-6, iNOS, COX-2, MRC1, Arg1, RARα, RARβ, and RARγ protein levels in liver were determined using western blot. Membranes were cut prior to antibody incubation; all available uncropped images are provided in the Supplementary Information. Original full-length images for certain replicates are unavailable due to loss of original acquisition files. Density analysis is shown in the right panel. (D) Protein levels of p38, p-p38 MAPK, ERK, p-ERK, JNK, p-JNK, PI3K, p-PI3K, Akt, p-Akt, STAT3, and p-STAT3 in the liver were determined using western blotting. Density analysis is shown in the lower panel. Results are presented as the means ± S.D. of six mice. Representative images of p-NF-κB staining (E), F4/80 staining (F), H&E staining (H), and Picro-Sirius Red staining (K) of liver tissues were shown. Quantitative analysis of p-NF-κB and F4/80 staining was performed using ImageJ software (G). The survival rate after adapalene administration in LPS-induced sepsis is shown (I). Hepatic mRNA and protein levels of fibrosis markers were determined (J). AD; adapalene, * P < 0.05, ** P < 0.01, and *** P < 0.001 vs. control; # P < 0.05, ## P < 0.01, and ### P < 0.001 vs. LPS alone.

Article Snippet: t-STAT3 , Cell Signaling , 9139 , Mouse , 1:1000.

Techniques: In Vivo, Injection, Quantitative RT-PCR, Western Blot, Incubation, Staining, Software, Control

Journal: Scientific Reports

Article Title: Adapalene, an RAR agonist, exerts anti-inflammatory effects by regulating macrophage polarization through RAR -mediated signaling pathways

doi: 10.1038/s41598-026-44454-z

Figure Lengend Snippet: In vivo anti-inflammatory effects of adapalene in HFD-induced obesity model. Adapalene (10 or 50 mg/kg) was orally administered once daily to HFD-induced obese mice ( n = 10 per group) for 3 weeks. On the last day of administration, serum and liver samples were collected from each mouse. (A) TNFα, IL-1β, IL-6, iNOS, COX-2, MRC1, Arg1, p38, p-p38 MAPK, ERK, p-ERK, JNK, p-JNK, RARα, RARβ, and RARγ protein levels in the liver were determined using western blotting. Density analysis is shown in the right panel. (B) PI3K, p-PI3K, Akt, p-Akt, STAT3, and p-STAT3 protein levels in the liver were determined using western blotting. Membranes were cut prior to antibody incubation; all available uncropped images are provided in the Supplementary Information. Original full-length images for certain replicates are unavailable due to loss of original acquisition files. Density analysis is shown in the lower panel. (C) TNFα, IL-6, IL-1β, COX-2, iNOS, MRC1, and Arg1 mRNA levels in the liver were determined using qRT-PCR. (D) Representative images of Oil Red O staining and Picro-Sirius Red staining (G) of liver tissues are shown. Results are presented as the means ± S.D. of eight mice. (E, F) Hepatic protein levels (E), mRNA levels of fibrosis markers (F) and serum ALT and AST levels (F) were determined. AD; adapalene, * P < 0.05, ** P < 0.01, and *** P < 0.001 vs. control; # P < 0.05, ## P < 0.01, and ### P < 0.001 vs. LPS alone.

Article Snippet: t-STAT3 , Cell Signaling , 9139 , Mouse , 1:1000.

Techniques: In Vivo, Western Blot, Incubation, Quantitative RT-PCR, Staining, Control

Journal: Scientific Reports

Article Title: Adapalene, an RAR agonist, exerts anti-inflammatory effects by regulating macrophage polarization through RAR -mediated signaling pathways

doi: 10.1038/s41598-026-44454-z

Figure Lengend Snippet: Proposed working model of the mechanism of action of adapalene. Adapalene produces anti-inflammatory effects through dual mechanisms involving the suppression of the M1-mediated inflammatory response and induction of the M2-mediated anti-inflammatory response. Both actions are mediated through RARβ activation, followed by MAPK and PI3K/Akt inactivation, and NF-κB inactivation (M1 response) as well as by STAT3 phosphorylation (M2 response).

Article Snippet: t-STAT3 , Cell Signaling , 9139 , Mouse , 1:1000.

Techniques: Activation Assay, Phospho-proteomics