XIST Inhibition Attenuates Calcium Oxalate Nephrocalcinosis-Induced Renal Inflammation and Oxidative Injury via the miR-223/NLRP3 Pathway

Figure 5

miR-223-3p reversed the effect of XIST on COM-induced renal tubular epithelial cell inflammation and oxidative injury. The levels of NLRP3, Caspase-1, and IL-1β in HK-2 cells cotransfected with si-XIST, the miR-223-3p inhibitor, or both were examined by Western blot (a) and qRT-PCR (b). The SOD expression (c), LDH release (d), MDA levels (e), and H₂O₂ generation (f) were detected in HK-2 cells transfected with si-XIST, the miR-223-3p inhibitor or si-XIST, and the miR-223-3p inhibitor in combination. (g) HK-2 necrosis was determined by flow cytometry. (h) The mitochondrial membrane potential was detected at Ex/Em wavelengths of 520/590 nm. Flow cytometry (i) and DCFH-DA (j) were used to assess the ROS production in HK-2 cells treated with si-XIST, the miR-223-3p inhibitor or si-XIST, and the miR-223-3p inhibitor in combination. The data are presented as the of three independent experiments. ; , versus the COM group, #, versus the COM+inhibitor 223 group, as determined by one-way ANOVA (a–j).

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