MALAT1在颅内动脉瘤炎症反应中的表达效应

The Expression Effect of MALAT1 in the Inflammatory Response of Intracranial Aneurysm

摘要: 目的：探讨长链非编码RNA转移相关肺腺癌转录本-1 (Metastasis-associated lung adenocarcinoma transcript-1, MALAT1)在颅内动脉瘤(Intracranial aneurysm, IA)炎症反应的表达效应及潜在作用。方法：收集临床IA患者的组织标本，并建立大鼠IA实验模型，通过荧光定量PCR检测MALAT1表达水平及WB检测相关炎症因子(MyD88, IL-6, TNF-α, NF-κB)，系统分析MALAT1及这些炎症因子在IA组织与非IA组织中的差异表达特征。结果：人体组织中，与非IA组相比，IA组MALAT1表达显著上调(P = 0.0005)；动物实验模型中，与假手术组比较，模型组大鼠IA组织MALAT1表达水平升高(P = 0.001)，且MyD88、IL-6、TNF-α、NF-κB炎症因子在动物实验模型中的表达较正常血管组织显著上调(P < 0.0001, P = 0.0132, P = 0.0006, P = 0.0005)。结论：MALAT1在IA组织中高度表达，并与MyD88等炎症因子在颅内动脉瘤中的表达水平呈正相关，这表明MALAT1可能参与了IA炎症反应的表达调控。

Abstract: Objective: To investigate the expression effects and potential roles of the long non-coding RNA MALAT1 in the inflammatory response of intracranial aneurysm (IA). Methods: Tissue specimens from clinical IA patients were collected, and a rat IA experimental model was established. The expression levels of MALAT1 were detected by qPCR, and related inflammatory factors (MyD88, IL-6, TNF-α, NF-κB) were measured by Western blot (WB). Systematic analysis was conducted to compare the differential expression characteristics of MALAT1 and these inflammatory factors between IA and non-IA tissues. Results: In human tissues, MALAT1 expression was significantly upregulated in the IA group compared to the non-IA group (P = 0.0005). In animal experimental models, MALAT1 expression levels were elevated in the IA tissues of rats in the model group compared to the sham surgery group (P = 0.001), and the expression levels of inflammatory factors such as MyD88, IL-6, TNF-α, and NF-κB inflammatory factors were significantly up-regulated in the animal experimental model compared with normal vascular tissue (P < 0.0001, P = 0.0132, P = 0.0006, P = 0.0005). Conclusion: MALAT1 is highly expressed in IA tissue and positively correlates with the expression levels of inflammatory factors such as MyD88 in intracranial aneurysms, suggesting that MALAT1 may be involved in the expression regulation of the inflammatory response in IA.