Key result
QSYQ reduces sepsis-induced cardiac microvascular and endothelial injury in preclinical models.
Why the study?
To determine whether QiShenYiQi Dripping Pills mitigate sepsis-induced cardiac microvascular leakage in rats and to elucidate the underlying mechanisms.
Does QSYQ reduce sepsis-induced cardiac microvascular hyperpermeability in rat models and HUVECs?
Does QSYQ reduce sepsis-induced cardiac microvascular hyperpermeability in rat models and HUVECs?
QSYQ ameliorates sepsis-induced cardiac endothelial barrier injury and microvascular leakage by enhancing mitochondrial ATP synthesis and preserving endothelial junctional proteins.
Objective To determine whether QiShenYiQi Dripping Pills (QSYQ) mitigate sepsis-induced cardiac microvascular leakage in rats and to elucidate the underlying mechanisms. Methods Sepsis was induced in Sprague–Dawley rats by cecal ligation and puncture (CLP). Rats were assigned to the Sham, CLP, and CLP + QSYQ groups. In vitro, an inflammatory endothelial injury model was established by stimulating human umbilical vein endothelial cells (HUVECs) with lipopolysaccharide (LPS). To examine the involvement of ATP synthesis, oligomycin (an ATP synthase inhibitor) was co-administered with QSYQ in vitro. Cardiac surface microcirculation imaging was performed to assess intravascular and extravascular distributions of FITC–dextran. Cardiomyocyte morphology and the ultrastructure of cardiac vascular endothelial junctions were evaluated using hematoxylin and eosin (H&E) staining and transmission electron microscopy, respectively. Junctional proteins (ZO-1, VE-cadherin, and claudin-5) were assessed by immunofluorescence and Western blotting. ELISA measured ATP synthase activity. Myocardial ATP and ADP levels were quantified by mass spectrometry. Endothelial monolayer permeability was evaluated using a Transwell assay. Results QSYQ significantly attenuated CLP-induced increases in myocardial microvascular permeability and endothelial barrier injury, which were associated with upregulation of ZO-1, VE-cadherin, and claudin-5 in cardiac tissue. Compared with the CLP group, QSYQ increased ATP, decreased ADP, and improved myocardial energy metabolism. In vitro, QSYQ reduced LPS-induced hyperpermeability in HUVECs and enhanced junctional protein expression. Co-treatment with oligomycin attenuated these effects of QSYQ. Conclusion QSYQ ameliorates sepsis-induced cardiac endothelial barrier injury and microvascular leakage, at least in part, by enhancing mitochondrial ATP synthesis and preserving endothelial junctional protein expression.
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Li et al. (2026) studied Sepsis-induced cardiac microvascular leakage. QiShenYiQi Dripping Pills (QSYQ) vs. Sham and CLP groups (in vivo); LPS alone (in vitro) was evaluated on Myocardial microvascular permeability and endothelial barrier injury. QiShenYiQi Dripping Pills significantly attenuated sepsis-induced myocardial microvascular permeability and endothelial barrier injury in rats and HUVECs.
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