Journal: Molecular Medicine Reports

Article Title: ST3Gal1 modulates intestinal barrier function and impacts human ulcerative colitis

doi: 10.3892/mmr.2025.13783

Figure Lengend Snippet: ST3Gal1 expression in inflamed IEC monolayers alters MUC2, TFF3, CDX2, STAT3 and p-STAT3 expression. ST3Gal1 knockdown in ST3Gal1-sh3/IEC significantly increased (A) MUC2, (B) TFF3 and (C) CDX2, but significantly reduced (D) STAT3 mRNA levels in the inflamed IEC monolayer. ST3Gal1 OE in ST3Gal1-OE/IEC significantly reduced (E) MUC2, (F) TFF3 and (G) CDX2 mRNA levels in the inflamed IEC monolayer. (H) ST3Gal1 OE in ST3Gal1-OE/IEC slightly decreased STAT3 mRNA levels in the inflamed IEC monolayer. (I) Western blotting showed no changes in protein expression in non-inflamed knockdown samples. (J) Western blotting showed that MUC2, TFF3 and CDX2 protein levels were increased, and p-STAT3 expression was decreased in the inflamed IEC monolayer comprising ST3Gal1-sh3/IEC. (K) Western blotting showed no notable changes in protein expression in non-inflamed OE samples. (L) Western blotting showed that MUC2, TFF3 and CDX2 protein levels were decreased, and p-STAT3 expression was increased in the inflamed IEC monolayer comprising ST3Gal1-OE/IEC. Data are presented as the mean ± SD. Statistical significance was assessed using one-way analysis of variance followed by Tukey's post-hoc test. *P<0.05 and **P<0.01. IEC, intestinal epithelial cell; sh, short hairpin; Ctr, control; OE, overexpression; MUC2, mucin 2; TFF3, trefoil factor 3; CDX2, homeobox protein CDX-2; p-, phosphorylated.

Article Snippet: Rabbit Polyclonal IgG to TFF3 , Proteintech Group, Inc. , 23277-1-AP , 1:1,000.

Techniques: Expressing, Knockdown, Western Blot, Control, Over Expression

Journal: Molecular Medicine Reports

Article Title: ST3Gal1 modulates intestinal barrier function and impacts human ulcerative colitis

doi: 10.3892/mmr.2025.13783

Figure Lengend Snippet: Comparison of (A) MUC2, (B) TFF3 and (C) CDX2 mRNA levels between non-lesional mucosa (n=44) and lesional mucosa (n=75) from distinct patients with ulcerative colitis. Correlations between (D) MUC2, (E) TFF3 and (F) CDX2 mRNA levels and ST3Gal1 expression. Data in A-C are presented as box and whisker plots, and those in D-F as scatter plots. Statistical significance for group comparisons in A-C was assessed using unpaired t-test. Correlation analyses in D-F were performed using Pearson's correlation coefficient. *P<0.05 and **P<0.01. Data were obtained from the GSE107499 dataset from the Gene Expression Omnibus database. *P<0.05 and **P<0.01. NS, not significant; MUC2, mucin 2; TFF3, trefoil factor 3; CDX2, homeobox protein CDX-2.

Article Snippet: Rabbit Polyclonal IgG to TFF3 , Proteintech Group, Inc. , 23277-1-AP , 1:1,000.

Techniques: Comparison, Expressing, Whisker Assay, Gene Expression

Journal: International Journal of Molecular Sciences

Article Title: Canagliflozin Attenuates Lipotoxicity in Cardiomyocytes by Inhibiting Inflammation and Ferroptosis through Activating AMPK Pathway

doi: 10.3390/ijms24010858

Figure Lengend Snippet: Canagliflozin promotes AMPK activation through upregulating LKB1, TAK1, and p-CaMKK2. HL-1 cells were stimulated with 0.1 mM PA for 24 h in the presence or absence of CAN (5 μg/mL), and the whole cell lysates from HL-1 cells were used for Western blotting analysis. ( A – C ) Effects of CAN on LKB1 and TAK1 in HL-1 cells. ( D – G ) Effects of CAN on the ratios of p-CaMKK2/CaMKK2 and p-AMPK/AMPK in HL-1 cells. Nor, normal control group; Mod, untreated PA control group; CAN, CAN-treated PA group. Data were expressed as mean ± SD ( n = 3). Differences were considered significant at p < 0.05 and highly significant at p < 0.01 (# p < 0.05, ## p < 0.01 vs. Nor; * p < 0.05 vs. Mod).

Article Snippet: The following were the specific primary antibodies used in the study: β-actin (1:5000, Mouse, A1978, Sigma-Aldrich, Saint Louis, MO, USA), COX-2 (1:1000, ET1610-23, HUABIO, Hangzhou, China), iNOS (1:1000, Rabbit, A3200, Abclonal Technology, Wuhan, China), LKB1 (1:1000, Rabbit, A2122, Abclonal Technology, Wuhan, China), TAK1 (1:1000, Rabbit, ET1705-14, HUABIO, Hangzhou, China), CaMKK2 (1:1000, Rabbit, A9899, Abclonal Technology, Wuhan, China), Phospho-CaMKK2 (Ser511) (1:1000, Rabbit, BD-PP1258, Biodragon, Suzhou, China), AMPKα (1:1000, Rabbit, 2532S, Cell Signaling Technology, Boston, MA, USA), Phospho-AMPKα (Thr172) (1:1000, Rabbit, 2535S, Cell Signaling Technology, Boston, MA, USA), NF-κB p65 (1:1000, Mouse, 6956S, Cell Signaling Technology, Boston, MA, USA), and Phospho-NF-κB p65 (Ser536) (1:1000, Rabbit, 3033S, Cell Signaling Technology, Boston, MA, USA).

Techniques: Activation Assay, Western Blot, Control