Your privacy, your choice

We use essential cookies to make sure the site can function. We also use optional cookies for advertising, personalisation of content, usage analysis, and social media.

By accepting optional cookies, you consent to the processing of your personal data - including transfers to third parties. Some third parties are outside of the European Economic Area, with varying standards of data protection.

See our privacy policy for more information on the use of your personal data.

for further information and to change your choices.

Skip to main content
Fig. 8 | Biological Procedures Online

Fig. 8

From: Deinococcus radiodurans-derived membrane vesicles protect HaCaT cells against H2O2-induced oxidative stress via modulation of MAPK and Nrf2/ARE pathways

Fig. 8

Effect of R1 DR2577 mutant strain (ΔDR2577) MVs isolated from ΔDR2577 (ΔDR2577 R1-MVs) against H2O2-induced oxidative stress. HaCaT cells were pre-processed with R1-MVs (30 μg/mL) or ΔDR2577 R1-MVs (30 μg/mL) for 12 h prior to exposure to H2O2 (0.3 mM) for 12 h. A Protective effect of MVs (R1 and ΔDR2577) against H2O2-induced oxidative stress in HaCaT cells assessed using annexin V/propidium iodide (PI) staining (PI+ cells, necrosis; AnnexinV+PI+ cells, late apoptosis; AnnexinV+ cells, early apoptosis). B Mitochondrial ROS scavenging effect of MVs (R1 and ΔDR2577) assessed using the Mitosox™ fluorescence probe in H2O2 exposed to HaCaT cells. ###p < 0.001 vs. control group; *p < 0.05, **p < 0.01, or ***p < 0.001 vs. H2O2-treated group; *p < 0.05, **p < 0.01, or ***p < 0.001 vs. H2O2/ΔDR2577 R1-MVs-treated group. The values show the mean ± SD (n = 4 samples) of three representative experiments

Back to article page