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. 2022 May 2;44(1):551–561. doi: 10.1080/0886022X.2022.2056486

Figure 5.

Figure 5.

miR-26a-5p targets IL-6 in LPS-induced septic AKI. An nti-miR-26a-5p agent (20 mg/kg) or negative control (NC) was administered to male C57BL/6 mice through tail vein injection two days before LPS injection. The mice were then injected intraperitoneally with 10 mg/kg LPS, and their kidney tissues were collected at 24 h after the LPS injection. Control mice were injected with normal saline. (A) Immunohistochemistry showing the repressive effect of miR-26a-5p on IL-6 expression, Scale bar: 50 μm. (B) The graph shows semiquantitative IL-6 expression detected by immunohistochemical; The data are expressed as the mean ± SD (n = 6), *p < 0.05. (C) The expression of IL-6 was detected by Western blot, and GAPDH was used as the internal control. (D) The predicted miR-26a-5p binding site in 3’UTR of IL-6 mRNA. (E) MicroRNA target reporter assay of the IL-6 3’UTR. The putative miR-26a-5p binding sequence of the IL-6 3’UTR was cloned into the pMIR-REPORT plasmid to analyze luciferase activity after transfection of the miR-26a-5p mimic transfection; the activity was compared to that in the negative control group. β-gal was cotransfected for normalization. The data are expressed as the mean ± SD (n = 4), *p < 0.05.