Basic & Clinical Medicine ›› 2026, Vol. 46 ›› Issue (3): 352-358.doi: 10.16352/j.issn.1001-6325.2026.03.0352

• Original Articles • Previous Articles     Next Articles

Knock-down MALAT1 reduces ox-LDL- induced-inflammation and cell damage of macrophages

SONG Ning1, LUO Junyi1, JI Wei1, LI Yanhong1, LI Xiaomei1*, YANG Yining2*   

  1. 1. Heart Center, the First Affiliated Hospital of Xinjiang Medical University, Urumqi 830054;
    2. Department of Cardiology, People′s Hospital of Xinjiang Uygur Autonomous Region, Urumqi 830001, China
  • Received:2025-04-23 Revised:2025-07-14 Online:2026-03-05 Published:2026-02-25
  • Contact: *yangyn5126@163.com; lixm505@163.com

Abstract: Objective To explore the role and potential mechanism of metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in inflammatory response and cell damage of macrophages induced by oxidized low density lipoprotein (ox-LDL). Methods THP-1 cells were induced to differentiate into macrophages by phorbol ester(PMA). Macrophages were co-cultured with ox-LDL to construct a cell injury model. Lipid accumulation was observed by Oil Red O staining microscopy. MALAT1 was knocked down by transfection of shRNA. The experimental group included control group, ox-LDL group, ox-LDL+shNC group and ox-LDL+shMALAT1 group. Total cholesterol and triglyceride in cells were measured. Apoptosis was detected by flow cytometry. The level of IL-6, TNFα and MCP-1 were detected by ELISA. The expression of NLRP3, RIPK1, caspase-8, p65 and SR-A was detected by RT-qPCR and Western blot. Results Compared with the control group, the cell lipid accumulation, total cholesterol and triglyceride contents, cell apoptosis, IL-6, TNFα and MCP-1 levels and the expression of NLRP3, RIPK1, caspase-8, p-p65 and SR-A increased significantly in ox-LDL group(P<0.05). Compared with ox-LDL group, ox-LDL+shMALAT1 group the contents of total cholesterol and triglyceride, apoptosis, IL-6, TNFα and MCP-1, and the expression of NLRP3, RIPK1, caspase-8, p-p65 and SR-A all significantly decreased(P<0.05). Conclusions MALAT1 may play an important role in ox-LDL-induced cell injury by regulating NLRP3 inflammatory corpuscles and related signal pathways. Knockdown of MALAT1 can significantly reduce the inflammatory reaction and cell damage induced by ox-LDL, which provides a potential target for the treatment of atherosclerosis.

Key words: atherosclerosis, metastasis-associated lung adenocarcinoma transcript 1(MALAT1), Nod-like receptor protein 3 (NLRP3), inflammation

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