Fig. 5: HBM-exo alleviated the injury of IECs cells by downregulating the abnormal HMGB3/JNK pathway induced by inflammatory injury. | Cell Death & Disease

Fig. 5: HBM-exo alleviated the injury of IECs cells by downregulating the abnormal HMGB3/JNK pathway induced by inflammatory injury.

From: MiR-200b in heme oxygenase-1-modified bone marrow mesenchymal stem cell-derived exosomes alleviates inflammatory injury of intestinal epithelial cells by targeting high mobility group box 3

Fig. 5

a HMGB3 protein of IECs in the Mock group, TNF-α group, TNF-α-exo, BM-exo, and HBM-exo groups was labeled using immunofluorescence. b, c QRT-PCR was used to detect the expression level of Hmgb3 and Jnk in each group (fold change to relative the Mock group, n = 4). d The negative control (Negative Con.) and HMGB3 overexpression (HMGB3-OE) IEC-6s were established by transfection of the negative control and the Hmgb3 overexpression plasmid; e The Cell Counting Kit-8 method was used to detect the relative cell viability (fold change relative to the Mock group, n = 4); f Annexin V-FITC/ PI-PE double staining was used to mark the proportion of early apoptosis (n = 4). g The protein expression levels of phosphorylated (p-) JNK, (cleaved) caspase-3, and ZO-1 proteins affected by HMGB3 were detected using western blotting (n = 4).*P < 0.05; BMMSCs Bone marrow mesenchymal stem cells; BM-exo BMMSCs co-culture system exosomes; DAPI 4,6-diamino-2-phenyl indole; Exo exosomes; FITC fluorescein isothiocyanate; HMGB3 high mobility group box 3; HO-1 heme oxygenase-1; HBM-exo HO-1/BMMSCs co-culture system exosomes; IECs, intestinal epithelial cells; JNK, C-Jun NH2-terminal kinase; PE phycoerythrin; PI propidium iodide; qRT-PCR quantitative real-time reverse transcription polymerase chain reaction; TNF-α tumor necrosis factor alpha; TNF-α-exo tumor necrosis factor alpha-treated IEC-6s system exosomes; ZO-1 Zona Occludens 1.

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