lncRNA HCP5 regulates inflammation and oxidative stress of neonatal sepsis via modulating miR-93-5p.

BACKGROUND

Due to the high sensitivity to pathogenic microorganisms, newborns showed a high incidence and mortality of sepsis. The dysregulation of non-coding RNAs may play a key role in the immune regulation of neonatal sepsis. This study aimed to evaluate the potential function of lncRNA human histocompatibility leukocyte antigen complex P5 (HCP5) in the inflammation and oxidative stress of neonatal and to disclose its potential molecular mechanism.

METHODS

The neonatal sepsis animal models were established with newborn rat pups by cecal ligation and perforation (CLP). The macrophage cells were induced by lipopolysaccharide (LPS) to mimic the sepsis injury. The expression of HCP5 was detected by polymerase chain reaction (PCR) and regulated by corresponding transfections. The inflammatory response was estimated by the levels of interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α (TNF-α) using enzyme-linked immunosorbent assay (ELISA); and the oxidative stress was assessed by the levels of malondialdehyde (MDA) and superoxide dismutase (SOD). The proliferation of macrophage cells was evaluated by the CCK8 assay.

RESULTS

HCP5 was significantly upregulated in neonatal sepsis rat models, of which the knockdown suppressed the inflammation and oxidative stress induced by CLP. In vitro, HCP5 was found to negatively regulate miR-93-5p in LPS-induced macrophage cells, which co-regulated the proliferation, inflammatory response, and oxidative stress in macrophage cells.

CONCLUSION

Upregulated HCP5 in neonatal sepsis rats regulated inflammation and oxidative stress, and it also modulated macrophage cell via regulating miR-93-5p.