Influence of lncRNA HOTAIR on acute kidney injury in sepsis rats through regulating miR-34a/Bcl-2 pathway.

Abstract

To study the regulatory effect of long non-coding ribonucleic acid (lncRNA) HOX transcript antisense RNA (HOTAIR) on acute kidney injury (AKI) in sepsis rats and its regulatory mechanism. The sepsis-induced AKI model was established in Sprague-Dawley (SD) male rats through cecal ligation puncture. A total of 30 SD rats were randomly divided into the control group, model group and lncRNA HOTAIR mimic group, with 10 rats in each group. Relative levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) in kidney tissues were detected via enzyme-linked immunosorbent assay (ELISA). Apoptosis of kidney tissues was detected via terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining. Moreover, the target gene of miR-34a was searched using the miRNA online database. The messenger RNA (mRNA) expression levels of miR-34a and B-cell lymphoma-2 (Bcl-2) were detected via Reverse Transcription-Polymerase Chain Reaction (RT-PCR). Compared with those in the control group, the rats in the model group showed injured pathological morphology of kidney, elevated contents of TNF-α and IL-1β, and apoptosis in kidney tissues. The target gene of miR-34a was Bcl-2, according to the miRNA online database. MiR-34a level in kidney tissues was upregulated, while the mRNA level of Bcl-2 significantly decreased in the model group. Compared with those in the model group, the pathological morphology of kidney tissues was improved, the content of TNF-α and IL-1β markedly declined, and the apoptotic rate of kidney tissues also reduced in lncRNA HOTAIR mimic group. The miR-34a level in kidney tissues decreased, while the Bcl-2 mRNA level remarkably increased in lncRNA HOTAIR mimic group. LncRNA HOTAIR overexpression can alleviate AKI in sepsis rats by inhibiting the apoptosis of kidney tissues by downregulating the miR-34a/Bcl-2 signaling pathway.