Histology and histopathology · 2026
Xuebijing alleviates septic myocardial injury by inhibiting ferroptosis mediated by the ICAM1/TLR signaling pathway.
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Meng Xiaoyan, Yan Xinming, Kan Chen, Li Haiquan, Han Dahe, Guo Yi, Xue Peng, Jiang Yuxin
Аннотация
BACKGROUND: Xuebijing (XBJ) has demonstrated efficacy in alleviating clinical symptoms in sepsis patients; however, its underlying mechanism requires further investigation.
METHODS: In this study, we established mouse and cardiomyocyte sepsis models using LPS. Cardiac pathological changes and ICAM1 expression were assessed through HE staining and immunohistochemistry. The expression of ICAM1, TFR1, ASCL4, TLR1, TBK1, and IFR7 was analyzed via PCR and western blotting. Cardiomyocyte survival and apoptosis were evaluated using the MTT assay and flow cytometry, respectively. Additionally, cTnI, BNP, CK-MB, IL-1β, IL-6, and TNF-α levels, along with GSH and MDA levels, were measured.
RESULTS: HE staining confirmed the successful construction of the LPS-induced mouse model. XBJ inhibited ICAM1 expression in myocardial tissue as well as cells. Overexpression of ICAM1 suppressed survival and GSH levels while promoting apoptosis along with increased levels of cTnI, BNP, CK-MB, IL-1β, IL-6, TNF-α, and MDA of myocardial cells. Furthermore, ICAM1 activated Toll-like receptor (TLR) signaling pathways. Conversely, ICAM shRNA exhibited opposite effects. XBJ inhibited the overactivated TLR signaling pathway, inflammatory responses, and apoptosis induced by ICAM overexpression.
CONCLUSION: XBJ ameliorates myocardial injury in sepsis by inhibiting the ICAM-regulated TLR signaling pathway.
METHODS: In this study, we established mouse and cardiomyocyte sepsis models using LPS. Cardiac pathological changes and ICAM1 expression were assessed through HE staining and immunohistochemistry. The expression of ICAM1, TFR1, ASCL4, TLR1, TBK1, and IFR7 was analyzed via PCR and western blotting. Cardiomyocyte survival and apoptosis were evaluated using the MTT assay and flow cytometry, respectively. Additionally, cTnI, BNP, CK-MB, IL-1β, IL-6, and TNF-α levels, along with GSH and MDA levels, were measured.
RESULTS: HE staining confirmed the successful construction of the LPS-induced mouse model. XBJ inhibited ICAM1 expression in myocardial tissue as well as cells. Overexpression of ICAM1 suppressed survival and GSH levels while promoting apoptosis along with increased levels of cTnI, BNP, CK-MB, IL-1β, IL-6, TNF-α, and MDA of myocardial cells. Furthermore, ICAM1 activated Toll-like receptor (TLR) signaling pathways. Conversely, ICAM shRNA exhibited opposite effects. XBJ inhibited the overactivated TLR signaling pathway, inflammatory responses, and apoptosis induced by ICAM overexpression.
CONCLUSION: XBJ ameliorates myocardial injury in sepsis by inhibiting the ICAM-regulated TLR signaling pathway.