Fig 2: Protein expression of JNK and Caspase3 in ovary after the supplementation of NAC and Sal. (A) JNK expression detected by immunohistochemistry (IHC) (Magnification: ×200). (B) Caspase3 expression detected by immunofluorescence (IF) (Magnification: ×200). Blue: DAPI, red: Caspase3. (C and D) Semiquantitative analysis of JNK and Caspase3. (E) Content of MDA in serum. (F) SOD activity in serum. **P < 0.01, ***P < 0.001: the 400 mg/kg ZnO NPs treatment group and the inhibitor groups versus the control group; #P< 0.05, ##P < 0.01, ###P < 0.001: the inhibitor groups versus the 400 mg/kg ZnO NPs treatment group.

Fig 3: Mechanism of TSH-induced tumor PD-L1 expression (A) KTC1 (left) and U87 (right) were treated with the culture supernatant of moDCs from patients with DTC and/or TSHR inhibitor (ML224). Whole-cell lysates were subjected for immunoblot analysis of PD-L1, HIF1a, ß-actin, phosphorylated, and total AKT, ERK, JNK, P38, P65. Representative immunoblot picture (up) and quantitative histogram (down) are shown. Expression of PD-L1 and HIF1a was calculated as the ratio between band intensity of these genes and ß-actin. Phosphorylation of five kinases was calculated as the ratio between band intensity of phosphorylated protein and total protein. (B–C) KTC1 (up) and U87 (down) were treated with TSH (B) or culture supernatant of moDCs (C) and four inhibitors. Representative histograms (left) and PD-L1 MFI (right) were shown. (D) Transcription factors (TF) enrichment in KTC1 treated with culture supernatant of moDCs based on RNA sequencing data sets. The scatter plot ranked TF from first with increasing enrichment and decreasing ChIP-X enrichment analysis 3 scores. TF from the AP-1 family (blue) and other PD-L1-related TF (red) were colored. (E) KTC1 (up) and U87 (down) were treated with the culture supernatant of moDCs from patients with DTC and/or TSHR inhibitor (ML224). Whole-cell lysates were subjected for immunoblot analysis of ß-actin, phosphorylated and total c-JUN, and STAT1. (F) Immunofluorescence staining of KTC1 (left) and U87 (right) for phosphorylated (down) and total (up) c-JUN. DTC, differentiated thyroid cancers; MFI, median fluorescence intensity; moDC, monocyte-derived dendritic cells; PD-L1, programmed death-ligand 1; TSH, thyroid-stimulating hormone; TSHR, TSH receptor.

Fig 4: OE blocked TLR4/MD2 complex formation in AKI mice. (A–K) Mice were administered OE (100, 200, 400 mg/kg) by gavage for 7 days followed by the intraperitoneal injection of LPS (10 mg/kg) and feeding for another 12 h. TLR4/MD2 (A,B), TLR4/MyD88 (C,D), and TLR4/TRIF (E,F) complex formation in mice kidneys were determined by a co-immunoprecipitation assay. Protein expression of p-JNK, JNK, p-ERK, ERK, p-p38, and p38 (G–J) in mice kidneys was analyzed by a western blotting analysis. The mRNA level of IFN-ß in mice kidney was determined by quantitative real time PCR analysis. Data presented as Means ± SD. * p < 0.05, ** p < 0.01 vs. control group; # p < 0.05, ## p < 0.01 vs. LPS group; ns, no significance.

Fig 5: The protective effects of CGA on TNF-a–induced apoptosis in hiPSC-CMs are mediated by inhibiting JNK. hiPSC-CMs were treated with CGA (0.1 µmol/L or 1 µmol/L) for 12 h prior to incubation with TNF-a for 24 h. The levels of phosphorylated JNK, JNK, phosphorylated p38, p38, phosphorylated ERK and ERK were determined by western blot (A). Quantitative analysis of phosphorylated ERK and ERK expression (B). Quantitative analysis of phosphorylated JNK and JNK(C). Quantitative analysis of phosphorylated p38 and p38 expression (D). Results are the means ± SD from three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001 significantly different between two groups