miRNA-1介导TRL4/NLRP3/NF-κB信号通路及细胞焦亡在间歇低氧肝损伤中的研究机制

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）是一种导致多系统多器官损伤的睡眠障碍性疾病，与肝脏损伤密切相关，已证实慢性间歇低氧(CIH)是OSAHS的病理生理基础。微小RNA（miRNA）是一种长度为18-24nt 的内源性非编码单链RNA，在转录后水平发挥广泛而重要的负调控作用。我们前期研究发现，慢性间歇性低氧可引起大鼠肝细胞损伤，且CIH大鼠肝细胞的miRNA-1基因表达上调。目前CIH所引起肝细胞损伤的机制尚不明确。本研究通过构建大鼠肝细胞CIH模型，检测TLR4/NLRP3/ NF-κB信号通路中关键分子的表达情况，试图从体内及体外两个水平阐明CIH引起肝细胞损伤可能的机制，为治疗CIH导致的OSAHS相关肝损伤提供新思路和新方法。

Obstructive sleep apnea hypopnea syndrome (OSAHS) is a sleep disorder that causes multiple system and multiple organ damage, chronic intermittent hypoxia (CIH) is the pathophysiological basis of its associated complications. MiRNAs, a class of 18–24 nucleotides, noncoding single-stranded RNAs that regulate gene function, leading to a significant negative regulation of relevant mRNAs to be translated into proteins. Our previous study found that the liver cell of mice was injuryed in CIH. and miRNA-1 expression was up-regulated in liver cell of CIH-treated rats. however, the role of chronic intermittent hypoxia-induced liver injury remains less defined. The study aims to detect the expression of key molecules in TLR4/NLRP3/ NF-κB signal pathway, in CIH-induced hepatocyte ferroptosis by using a CIH model of hepatocyte. It will provide a potential target for novel therapeutics to treat liver injury associated OSAHS.