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. 2021 Nov 1;9:673993. doi: 10.3389/fcell.2021.673993

FIGURE 5.

FIGURE 5

Role of ROS/NF-κB signaling pathway in H. pylori-derived OMVs-mediated effects in HUVECs. (A) ROS were determined by dihydroethidium staining in HUVECs treated with H. pylori-derived OMVs (10 μg/mL) for 24 h (n = 4, #P < 0.01 vs. control). (B–D) HUVECs were administrated with control (vehicle), OMVs (10 μg/mL), LPS-depleted OMVs or CagA-negative OMVs for 24 h. The expressions of SOD2 and gp91phox (B), p65 (C), IκBα (D) were determined by immunoblotting (n = 3, *P < 0.05 vs. OMVs or #P < 0.01 vs. control). (E) HUVECs were treated with control (vehicle), OMVs (10 μg/mL), OMVs + TEMPOL, and OMVs + BAY11-7082 for 24 h. The expression of cleaved-caspase-3 and total caspase-3 were determined by immunoblotting (n = 6, *P < 0.05 vs. OMVs or #P < 0.01 vs. control). (F) Proliferation of HUVECs were assayed by CCK8 after treatment with vehicle, OMVs (10 μg/mL), OMVs + TEMPOL, and OMVs + BAY11-7082 for 24 h (n = 17, *P < 0.05 vs. OMVs or #P < 0.01 vs. control). (G,H) ApoE–/– mice or control mice were intragastrically administered with vehicle or H. pylori-derived OMVs for 4 weeks. Levels of IL-6 (G) and TNF-α (H) were determined by ELISA (n = 5, #P < 0.05 vs. control).