MiR-20a Promotes kidney injury in sepsis rats through autophagy.

The aim of this work was to study the effects of micro ribonucleic acid (miR)-20a on acute kidney injury (AKI) in sepsis rats and its key molecular mechanism. Sprague-Dawley rats were randomly divided into healthy rat group (H group, n=3), sham group (S group, n=3), sepsis rat group (D group, n=3), sepsis rat + negative control transfection group (N group, n=3) and sepsis rat + miR-20a inhibitor transfection group (M group, n=3). At 6 h, 12 h and 24 h, serum creatinine (Scr) and blood urea nitrogen (BUN) were detected, the changes in miR-20a expression in kidney tissues were determined via reverse transcription-polymerase chain reaction (RT-PCR), the expression of autophagy marker protein microtubule-associated protein 1 light chain 3 (LC3) was measured via Western blotting, and the inflammatory cell infiltration in kidney tissues was detected using hematoxylin-eosin (HE) staining. There was no obvious change in each index in S group compared with H group. D group, N group and M group had higher levels of Scr, BUN and LC3 in kidney tissues than S group. The levels of Scr, BUN and LC3 in kidney tissues were lower in M group than those in N group. MiR-20a may cause AKI in sepsis rats via activating autophagy.
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