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

Figure 4.

Figure 4

miR-98-5p/IGF1R axis regulates oxidative stress and inflammation in PRKs induced by Ang II. (A) Cell Counting Kit-8 analysis determined the combined effects of miR-98-5p-MVs and IGF1R on the cell viability of PRKs treated with Ang II (n=3). (B and C) Flow cytometry analysis determined the combined effects of miR-98-5p-MVs and IGF1R on Ang II-induced ROS generation in PRKs (n=3). ELISA analysis determined the combined effect of miR-98-5p-MVs on the levels of (D) MDA, (E) GSH and (F) SOD produced by PRKs treated with Ang II (n=3). ELISA analysis determined the combined effects of miR-98-5p-MVs and IGF1R on the levels of (G) IL-1β, (H) IL-6 and (I) TNF-α secreted by PRKs treated with Ang II (n=3). *P<0.05 vs. Ang II; #P<0.05 vs. mimic-MVs + ov-NC. IGF1R, insulin-like growth factor 1 receptor; 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; ov, overexpression; miR, microRNA.