新生儿高胆红素血症可进展为急性胆红素脑病(ABE),构成短期和长期健康风险。尽管广泛的研究鉴定了许多mRNA,lncRNAs,circRNAs,和与脑损伤相关的miRNA,它们在新生儿胆红素诱导的脑损伤中的作用仍然难以捉摸。本研究采用全转录组测序来确定新生ABE大鼠模型中差异表达(DE)RNA谱,其次是生物信息学分析。建立了时间序列竞争内源性RNA(ceRNA)调控网络,并通过定量实时聚合酶链反应(qRT-PCR)验证了9种任意选择的RNA的表达趋势。与对照组相比,我们鉴定了595、888和1448个DEmRNAs;22、37和37个DEmiRNAs;1945、1869和1997年DElncRNAs;和31、28和36个DEcircRNAs,12h,24小时,分别。主要是,这些DERNA有助于与炎症相关的生物学功能和途径,豁免权,新陈代谢,细胞死亡,和神经发育调节。此外,我们基于时间序列构建了DElncRNA/circRNA-DEmiRNA-DEmRNA的ceRNA网络。所选择的9种RNA的qRT-PCR表达趋势通常与RNA-seq结果相似。这项研究独特地描绘了ABE中mRNA和非编码RNA的时间表达模式,建立ceRNA网络并确定胆红素诱导海马损伤的潜在分子机制。尽管如此,需要进一步的研究来证实这些在人类中的发现。
Hyperbilirubinemia in newborns may progress to acute bilirubin encephalopathy (ABE), posing short- and long-term health risks. Despite extensive research identifying numerous mRNAs, lncRNAs, circRNAs, and miRNAs associated with brain injury, their roles in neonatal bilirubin-induced brain injury remain elusive. This study employed whole-transcriptome sequencing to ascertain the differentially expressed (DE) RNA profiles in a newborn ABE rat model, followed by bioinformatic analysis. A time-series competing endogenous RNA (ceRNA) regulatory network was established, and the expression trends of 9 arbitrarily chosen RNAs were verified through quantitative real-time polymerase chain reaction(qRT-PCR). In comparison with the control group, we identified 595, 888, and 1448 DE mRNAs; 22, 37, and 37 DE miRNAs; 1945, 1869, and 1997 DE lncRNAs; and 31, 28, and 36 DE circRNAs at 6 h, 12 h, and 24 h, respectively. Predominantly, these DERNAs contribute to biological functions and pathways associated with inflammation, immunity, metabolism, cell death, and neurodevelopmental regulation. Moreover, we constructed ceRNA networks of DE lncRNA/circRNA-DE miRNA-DE mRNA based on time series. The qRT-PCR expression trends for the selected 9 RNAs were generally similar to the RNA-seq outcomes. This investigation uniquely delineated the temporal expression patterns of mRNA and non-coding RNA in ABE, establishing ceRNA networks and identifying potential molecular mechanisms underlying bilirubin-induced hippocampal damage. Nonetheless, further studies are warranted to corroborate these findings in humans.