European journal of pharmacology · 2026
Selenomethionine regulates macrophage polarization through mitochondrial dynamics via NF-κB signaling to attenuate sepsis-induced cardiomyopathy.
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Zhou Xu, Zhao Jiling, Yi Jiaolong, Liu Yuwei, Deng Bingqing, Xia Zhonnan, Wu Heng, Liu Jie, Liu Mengying, Lei Yuhua, Zhu Xiaoqin, Li Yuyu, Hu Jiaxin
Аннотация
BACKGROUND: Sepsis frequently leads to multiple organ dysfunction, among which sepsis-induced cardiomyopathy (SIC) is a severe complication associated with high mortality and limited targeted therapies. Selenomethionine (SeMet) possesses potent antioxidant and anti-inflammatory properties; however, its role in SIC remains unclear.
METHODS AND RESULTS: SIC models were established in C57BL/6J mice by intraperitoneal injection of LPS at 10 mg/kg or by cecal ligation and puncture (CLP). Mice were pretreated with SeMet (7.5 μg/20 g) by gavage for one week, followed by LPS challenge for 24 h. Cardiac function was evaluated by echocardiography, including left ventricular fractional shortening (LVFS), left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDd), and left ventricular end-systolic diameter (LVEDs). SeMet improved cardiac function in SIC mice, and this protective effect was associated with NF-κB signaling-mediated regulation of macrophage polarization. To further investigate the anti-inflammatory effects of SeMet in vitro, RAW264.7 macrophages were treated with 1 μM SeMet for 24 h and then stimulated with 1 μg/mL LPS for another 24 h. Immunofluorescence staining, Western blotting, and ELISA were performed to evaluate inflammatory responses and the underlying mechanisms. The results showed that SeMet modulated macrophage polarization through the NF-κB signaling pathway and exerted significant anti-inflammatory effects.
CONCLUSIONS: SeMet regulates macrophage polarization by inhibiting activation of the NF-κB signaling pathway, thereby alleviating sepsis-induced cardiac dysfunction in SIC mice.
METHODS AND RESULTS: SIC models were established in C57BL/6J mice by intraperitoneal injection of LPS at 10 mg/kg or by cecal ligation and puncture (CLP). Mice were pretreated with SeMet (7.5 μg/20 g) by gavage for one week, followed by LPS challenge for 24 h. Cardiac function was evaluated by echocardiography, including left ventricular fractional shortening (LVFS), left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDd), and left ventricular end-systolic diameter (LVEDs). SeMet improved cardiac function in SIC mice, and this protective effect was associated with NF-κB signaling-mediated regulation of macrophage polarization. To further investigate the anti-inflammatory effects of SeMet in vitro, RAW264.7 macrophages were treated with 1 μM SeMet for 24 h and then stimulated with 1 μg/mL LPS for another 24 h. Immunofluorescence staining, Western blotting, and ELISA were performed to evaluate inflammatory responses and the underlying mechanisms. The results showed that SeMet modulated macrophage polarization through the NF-κB signaling pathway and exerted significant anti-inflammatory effects.
CONCLUSIONS: SeMet regulates macrophage polarization by inhibiting activation of the NF-κB signaling pathway, thereby alleviating sepsis-induced cardiac dysfunction in SIC mice.