Abstract:
Maternal inflammation can lead to premature birth and fetal brain damage.In this study, Pregnant mice were intraperitoneally injected with lipopolysaccharide (LPS) to establish a preterm brain injury model induced by inflammation in mice. Lentivirus-mediated circ_19038 overexpression vector (LV-circ_19038) and LV-lnc-AK016022 were administered alone or jointly . H&E staining and electron microscopy were used to analyze structural damage in cerebral white matter of neonatal mice, immunofluorescence and RT-qPCR were used to explore glial activation and inflammatory factor expression, and immunohistochemistry was conducted to detect the expression of myelin basic protein (MBP). Behavioral tests were carried out to evaluate the long-term cognitive and motor functions of mice. We found that the expression levels of circ_19038 and lnc-AK016022 in the brain tissues of preterm mice were significantly lower than those of full-term healthy mice. Overexpression of circ_19038 or/and lnc-AK016022 promoted remyelination and alleviated white matter structural damage, neuroinflammation, and long-term cognitive and motor deficits in preterm mice, and the combined effect of circ_19038 and lnc-AK016022 showed better results.
Audience TakeWay:
- We have revealed the synergistic regulation of circRNA and lncRNA in the preterm brain injury ?which provided a new reference for exploring the mechanism of brain injury.
