miR-26a-5p Attenuates Oxidative Stress and Inflammation in Diabetic Retinopathy through the USP14/NF-κB Signaling Pathway

Figure 3

HG-evoked activation of NF-κB signaling was suppressed by USP14 knockdown or miR-26a-5p elevation. (a) Western blotting was conducted to quantify protein levels of USP14, p-IκBα, IκBα, NF-κB (cytoplasm), GAPDH, NF-κB (nuclear), and histone H3 in Müller cells of the control, HG, HG + sh-NC, and HG + sh-USP14 groups. (b) The binding site between miR-26a-5p and USP14 3′UTR (from starBase). (c) Luciferase reporter assay was carried out for confirming the interaction between miR-26a-5p and USP14 3′UTR. (d) RT-qPCR was performed to detect USP14 expression in Müller cells of the control, HG, HG + NC mimics, and HG + miR-26a-5p mimics groups. (e) Western blotting was conducted for quantifying the protein levels of USP14, p-IκBα, IκBα, NF-κB (cytoplasm), GAPDH, NF-κB (nuclear), and histone H3 in Müller cells of the control, HG, HG + NC mimics, and HG + miR-26a-5p mimics groups. (f) Immunofluorescence staining was performed to visualize the intensity of NF-κB in Müller cells of the control, HG, HG + NC mimics, and HG + miR-26a-5p mimics groups. , , and .

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