ArticleHistology and histopathology2026
Xuebijing alleviates septic myocardial injury by inhibiting ferroptosis mediated by the ICAM1/TLR signaling pathway.
Article in Histology and histopathology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Ferroptosis in heatstroke: Mechanisms and therapeutic perspectives (Review).International journal of molecular medicine · 2026Review
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Authors and funding
8 authors.
Funding
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Abstract
backgroundXuebijing (XBJ) has demonstrated efficacy in alleviating clinical symptoms in sepsis patients; however, its underlying mechanism requires further investigation.
methodsIn 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.
resultsHE 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.
conclusionXBJ ameliorates myocardial injury in sepsis by inhibiting the ICAM-regulated TLR signaling pathway.
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