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. 2022 Sep 29;24(5):702. doi: 10.3892/etm.2022.11638

Figure 2.

Figure 2

miR-98-5p-MVs inhibit Ang II-induced oxidative stress and the secretion of inflammatory cytokines in PRKs. (A) PKH26-labeled miR-98-5p-MVs successfully fused with PRKs (magnification, x100). (B) Cell Counting Kit-8 analysis determined the effects of miR-98-5p-MVs on the cell viability of PRKs treated with Ang II (n=3). (C and D) Flow cytometry analysis determined the effect of miR-98-5p-MVs on the levels of Ang II-induced ROS production in PRKs (n=3). ELISA analysis determined the effect of miR-98-5p-MVs on the levels of (E) MDA, (F) GSH and (G) SOD in PRKs treated with Ang II (n=3). ELISA analysis determined the effect of miR-98-5p-MVs on the levels of secreted (H) IL-1β, (I) IL-6 and (J) TNF-α in PRKs treated with Ang II (n=3). *P<0.05 vs. mimic NC; #P<0.05 vs. inhibitor NC. Ang II, angiotensin II; ROS, reactive oxygen species; EPCs, endothelial progenitor cells; PRKs, primary renal kidney cells; MVs, microvesicles; MDA, malondialdehyde; GSH, glutathione; SOD, superoxide dismutase; NC, negative control; miR, microRNA.