Journal: Molecular Medicine Reports

Article Title: Atractylenolide III inhibits epithelial-mesenchymal transition in small intestine epithelial cells by activating the AMPK signaling pathway

doi: 10.3892/mmr.2022.12614

Figure Lengend Snippet: Effect of ATL-III on the activity of IEC-6 cells. (A) Chemical structure of ATL-III. (B) Effect of ATL-III on the activity of IEC-6 cells was detected using an MTT assay. ATL-III, atractylenolide III.

Article Snippet: IEC-6 (rat small intestinal epithelial) cells were purchased from Merck-KGaA.

Techniques: Activity Assay, MTT Assay

Journal: Molecular Medicine Reports

Article Title: Atractylenolide III inhibits epithelial-mesenchymal transition in small intestine epithelial cells by activating the AMPK signaling pathway

doi: 10.3892/mmr.2022.12614

Figure Lengend Snippet: ATL-III inhibits the invasion and migration of IEC-6 cells induced by TGF-β1. (A) Cell morphology after TGF-β1 treatment was observed under a microscope. (B) Cell morphology after ATL-III treatment was observed under a microscope. Magnification, ×200. (C) Migration of IEC-6 cells was detected using a wound healing assay. (D) Cell invasion was detected using a Transwell assay. Histograms of cell (E) migration and (F) invasion rates. (G) Expression level of MMP9, as detected via western blotting. Magnification, ×100. ***P<0.001 vs. control group; ## P<0.01, ### P<0.001 vs. TGF-β1 group; n≥3. ATL-III, atractylenolide III.

Article Snippet: IEC-6 (rat small intestinal epithelial) cells were purchased from Merck-KGaA.

Techniques: Migration, Microscopy, Wound Healing Assay, Transwell Assay, Expressing, Western Blot, Control

Journal: Molecular Medicine Reports

Article Title: Atractylenolide III inhibits epithelial-mesenchymal transition in small intestine epithelial cells by activating the AMPK signaling pathway

doi: 10.3892/mmr.2022.12614

Figure Lengend Snippet: ATL-III inhibits the EMT of IEC-6 cells induced by TGF-β1. (A) Expression levels of protein associated with EMT, as detected via western blotting. (B) Expression levels of N-cadherin and (C) E-cadherin were detected using an immunofluorescence assay. Magnification, ×200. ***P<0.001 vs. control group; ## P<0.01, ### P<0.001 vs. TGF-β1 group; n≥3. ATL-III, atractylenolide III; EMT, epithelial-mesenchymal transition; ZO-1, zonula occludens-1.

Article Snippet: IEC-6 (rat small intestinal epithelial) cells were purchased from Merck-KGaA.

Techniques: Expressing, Western Blot, Immunofluorescence, Control

Journal: Molecular Medicine Reports

Article Title: Atractylenolide III inhibits epithelial-mesenchymal transition in small intestine epithelial cells by activating the AMPK signaling pathway

doi: 10.3892/mmr.2022.12614

Figure Lengend Snippet: ATL-III activates the AMPK signaling pathway in IEC-6 cells. (A) Expression levels of p-AMPK and AMPK in the groups treated with different concentrations of ATL-III were measured using western blotting. (B) Expression levels of p-AMPK and AMPK in the groups treated with TGF-β1 and different concentrations of ATL-III were measured using western blotting. (C) Chemical structure of compound C. (D) Expression levels of p-AMPK and AMPK in the groups treated with TGF-β1, ATL-III and compound C were detected using western blotting. *P<0.05, ***P<0.001 vs. control group; ### P<0.001 vs. TGF-β1 group; △△P<0.01 vs. TGF-β1 + ATL-III (20 µmol/l) group; n≥3. ATL-III, atractylenolide III; AMPK, AMP-activated protein kinase; p-, phosphorylated; t-, total.

Article Snippet: IEC-6 (rat small intestinal epithelial) cells were purchased from Merck-KGaA.

Techniques: Expressing, Western Blot, Control

Journal: Molecular Medicine Reports

Article Title: Atractylenolide III inhibits epithelial-mesenchymal transition in small intestine epithelial cells by activating the AMPK signaling pathway

doi: 10.3892/mmr.2022.12614

Figure Lengend Snippet: ATL-III inhibits the invasion, migration and EMT process of IEC-6 cells induced by TGF-β1 by activating the AMPK signaling pathway. (A) Cell migration, as determined using a wound healing assay. (B) Cells invasion was detected using a Transwell assay. Magnification, ×100. Histograms of cell (C) migration and (D) invasion rates. (E) Expression levels of MMP9 and proteins associated with EMT, as detected via western blotting. (F) N-cadherin and (G) E-cadherin expression was detected using an immunofluorescence assay. Magnification, ×200. ***P<0.001 vs. control group; ### P<0.001 vs. TGF-β1 group; △P<0.05, △△P<0.01 vs. TGF-β1 + ATL-III (20 µmol/l) group; n≥3. ATL-III, atractylenolide III; EMT, epithelial-mesenchymal transition; AMPK, AMP-activated protein kinase; ZO-1, zonula occludens-1.

Article Snippet: IEC-6 (rat small intestinal epithelial) cells were purchased from Merck-KGaA.

Techniques: Migration, Wound Healing Assay, Transwell Assay, Expressing, Western Blot, Immunofluorescence, Control

Journal:

Article Title: Polarized fibronectin secretion induced by adenosine regulates bacterial-epithelial interaction in human intestinal epithelial cells

doi: 10.1042/BJ20040021

Figure Lengend Snippet: T84 monolayers grown in DMEM supplemented with 10% FBS were serum starved for 24 h in 0.5% FBS. Adenosine (Ado; 100 μM) was then added to the apical (Ap) or basolateral (Bl) compartment. After an incubation period of 24 h, culture media in the apical or basolateral compartments were collected and processed for Western blotting to determine FN secretion. Protein bands in the autoradiogram shown in (A) were quantified by scanning densitometry, and densities relative to vehicle-treated controls are shown in the histogram to illustrate the alterations in band intensities. The data are representive of three separate experiments. (B) Confocal imaging of adenosine-induced FN in intestinal epithelial monolayer. Serum starved T84 cells (0.5% FBS, 24 h) were stimulated with apical or basolateral adenosine (100 μM) for 24 h, after which they were fixed and stained with anti-FN antibody followed by FITC-conjugated secondary antibody and counterstained with rhodamine/phalloidin, as described in the Experimental section. Vertical sections were taken off the monolayers to define the top (0 μm) and the bottom of the monolayer (18–20 mm). Shown here are ‘en face’ (x–y) images taken at the level of apical (1.2 μm above the level of tight junction), mid- (6 μm below the level of tight junction) and basal (18–20 μm, at the level of the stress fibres) pole of the epithelial monolayer.

Article Snippet: To determine if adenosine modulates FN secretion and whether this modulation is polarized, confluent monolayers of intestinal epithelial T84 and IEC-6 cells, grown in tissue culture inserts (Corning, Acton, MA, U.S.A.), were stimulated via the apical or basal surface with adenosine (0–100 μM), and conditioned media were analysed by Western blot analysis to examine the steady-state level of FN protein.

Techniques: Incubation, Western Blot, Imaging, Staining

Journal:

Article Title: Polarized fibronectin secretion induced by adenosine regulates bacterial-epithelial interaction in human intestinal epithelial cells

doi: 10.1042/BJ20040021

Figure Lengend Snippet: IEC-6 monolayers were stimulated with apical or basolateral adenosine (Ado; 100 μM). Conditioned media were collected at indicated times after adenosine treatment and FN was measured as described in the Experimental section. Protein bands in the autoradiograms were quantified by scanning densitometry and histograms of the densities relative to vehicle-treated controls are shown to illustrate the alterations in band intensities. The data are representative of the responses observed in two separate experiments carried out in duplicate.

Article Snippet: To determine if adenosine modulates FN secretion and whether this modulation is polarized, confluent monolayers of intestinal epithelial T84 and IEC-6 cells, grown in tissue culture inserts (Corning, Acton, MA, U.S.A.), were stimulated via the apical or basal surface with adenosine (0–100 μM), and conditioned media were analysed by Western blot analysis to examine the steady-state level of FN protein.

Techniques: