Introduction:
The present study examined the effects and mechanisms underlying long non-coding RNA (lncRNA) UBE2R2-AS1 in diabetes-induced renal injury.

Material and methods:
High glucose was used to imitate diabetes-induced renal injury in a cell model. Cell apoptosis rate was measured using flow cytometry, tumour necrosis factor-a (TNF-a) and interleukin-6 (IL-6) concentrations were evaluated using ELISA, and relative protein expression and amount were measured using western blot (WB) analysis and immunofluorescence, respectively. Correlations between lncRNA UBE2R2-AS1, miRNA-877-3p and TLR4 were analysed using the luciferase reporter assay.

Results:
Cell apoptosis rate and TNF-a and IL-6 concentrations were significantly higher (p < 0.001) in the high glucose (model) group compared with those of the Control group (CG) group. Following shRNA knockdown of lncRNA UBE2R2-AS1, the cell apoptosis rate and TNF-a and IL-6 concentrations were significantly lower (p < 0.001, respectively) compared with those of the model group. However, under high-glucose conditions, shRNA knockdown of UBE2R2-AS1 and miRNA-877-3p significantly increased (p < 0.001) the cell apoptosis rate as well as TNF-a and IL-6 concentrations compared with the shRNA UBE2R2-AS1 knockdown group. WB and immunofluorescence analysis showed that toll-like receptor 4 (TLR4)/myeloid differentiation factor 88 (MyD88)/nuclear factor kB (p65) (NF-kB(p65)) pathway proteins were significantly stimulated in the model group compared with those in the CG, whereas shRNA transfection with miRNA-877-3p stimulation suppressed the TLR4/MyD88/NF-kB(p65) pathway.

Conclusions:
Knockdown of lncRNA UBE2R2-AS1 improves diabetes-induced renal injury via regulation of the miRNA-877-3p/TLR4 axis in vitro.