Alpinia officinarum Hance extract relieved sepsis-induced myocardial ferroptosis and inflammation by inhibiting lncRNA MIAT/TRAF6/NF-κB axis

被引:0
|
作者
Shi, Yao [1 ]
Yang, Xiaobo [1 ,2 ]
Jiang, Hong
Wu, Shanxia [1 ]
Hong, Yan [1 ]
Su, Wei [1 ]
Wang, Xuan [1 ]
机构
[1] Huazhong Univ Sci & Technol, Cent Hosp Wuhan, Tongji Med Coll, Dept Pediat,Key Lab Mol Diag Hubei Prov, Wuhan, Peoples R China
[2] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Ophthalmol, 1277 Jiefang Ave, Wuhan, Hubei, Peoples R China
关键词
Alpinia officinarum Hance; sepsis; ferroptosis; MIAT; TRAF6/NF-kappa B axis; CURCUMIN; ANTIOXIDANT;
D O I
10.15586/aei.v52i5.1035
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Sepsis is generally triggered by a dysfunctional host response to infection, and it can result in life-threatening organ dysfunction. Alpinia officinarum Hance (AO) exhibits regulatory functions in some diseases. However, whether AO extract (AOE) plays a promoting role in sepsis- triggered myocardial injury is unclear. This study was aimed at investigating the regulatory effects of AOE on myocardial ferroptosis and inflammation in sepsis, and the regulation effects on the lncRNA MIAT/TRAF6/NF-kappa B axis. Lipopolysaccharide (LPS) was used to treat mice for establishing an in vivo sepsis model. The pathological changes in heart tissues were observed through hematoxylin-eosin (HE) staining. The levels of CK-MB, cTnl, MDA, SOD, IL-1 beta, IL-18, IL-6, and TNF-alpha in serum were detected through enzyme-linked immunosorbent assay (ELISA). The level of Fe2+ was assessed, and the protein expressions (ACSL4, GPX4, TRAF6, p-P65, and P65) were examined through western blot. The expressions of lncRNA MIAT and TRAF6 were measured through real-time quantitative polymerase chain reaction (RT-qPCR). Our results demonstrated that AOE treatment ameliorated sepsis-triggered myocardial damage by reducing the disordered cardiomyocytes, the destroyed sarcolemma, and the CK-MB and cTnl levels. In addition, AOE treatment inhibited sepsis-induced myocardial ferroptosis and inflammation by regulating Fe2+, ACSL4, GPX4, IL-1 beta, IL-18, IL-6, and TNF-alpha levels. Moreover, the improvement effect of AOE was strengthened with the increase in the dose of AOE (25, 50, 100 mg/kg). It was also revealed that AOE treatment retarded the lncRNA MIAT/TRAF6/NF-kappa B axis. Rescue assays manifested that overexpression of MIAT reduced the cardioprotective effect of AOE. In conclusion, AOE relieved sepsis-induced myocardial ferroptosis and inflammation by inhibiting lncRNA MIAT/TRAF6/NF-kappa B axis. These findings may provide a potential therapeutic drug for the treatment of sepsis. (c) 2024 Codon Publications. Published by Codon Publications.
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收藏
页码:21 / 28
页数:8
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