Abstract:

Objective To investigate the mechanism ofaction ofmiR⁃216a on acute kidney injury in septic ratsvia NF⁃κB signaling pathway. Methods Forty SD rats were selected，and a rat model was established by cecal ligation and puncture. The rates were randomly divided into asham⁃operation group，model group，miR⁃NC group， and miR⁃216a group，10 for each group. The pathologicalchangesin thekidneys were observed. RT⁃PCR was used to detect expression of miR⁃216a in the ratkidney tissues in each group；serum levels of biochemical indexes were detected by automatic biochemical analyzer；levels of inflammatory factors in each group were detected by ELISA； and expression of murine NF ⁃ κB pathway ⁃ related protein was detected by WB. Results In the sham ⁃operation group，no abnormal kidney tissue structure developed；in the model and the miR ⁃NC groups，the kidney tissues wereaccompanied by inflammatory infiltration and widened interstitium；andin the miR⁃216a group，inflammatory infiltration and glomerular lesions were alleviated. As compared with the sham⁃operationgroup，expression levels of miR⁃216a inthe kidney tissues were lower in the model group andthemiR⁃NC group，and as compared with the miR⁃NC group，expression levels of miR⁃216a inthe kidney tissue were higher in the miR⁃216a group.As compared with the sham⁃operationgroup，serum levels of Scr，BUN and KIM⁃1 were higher in the model group and the miR⁃NC group while lower in the miR⁃216a groupascompared with the miR⁃NC group（P < 0.05）. As compared to the sham⁃ operation group，serum levels of TNF⁃α，IL⁃6，and IL⁃1β were higher in the model groupand miR⁃NC group，but⁃ lower in themiR ⁃ 216a group ascompared to miR ⁃ NC group（P < 0.05）. In comparison withthe sham ⁃ operation group，expressions of NF⁃κB p65，p⁃NF⁃κB and p65 were higher inthemodel groupand miR⁃NC group，while thoseexpressionswerelower in the miR⁃216a groupthan in the miR⁃NC group（P < 0.05）. Conclusions miR⁃216a over⁃ expression reduced inflammation levels and ameliorated renal injury in septic rats，possibly through regulation of the NF⁃κB signaling pathway.

Key words:

miR?216a, NF?κB signaling pathway, sepsis, acute kidney injury