Objective This study aimed to evaluate the therapeutic potential of gymnoside I, a bioactive compound isolated from Bletilla striata , in the management of hemorrhage-related disorders and to elucidate its underlying mechanisms of action. Methods A multi-tiered experimental strategy was employed. In vivo assays assessed bleeding and clotting times in normal mice and examined gymnoside I’s effects on heparin-induced coagulopathy. Pharmacokinetic–pharmacodynamic (PK–PD) modeling was conducted to characterize time- and concentration-dependent effects. Network pharmacology was used to identify intersecting genes between gymnoside I and hemorrhagic diseases, followed by molecular docking and biolayer interferometry to validate protein interactions. Results Gymnoside I significantly reduced bleeding and clotting times in normal mice and partially reversed heparin-induced coagulopathy by improving thrombin time, platelet count, thromboxane B 2 , and fibrinogen levels. PK–PD modeling revealed distinct hysteresis loops, indicating delayed stimulation and potential feedback regulation. Network pharmacology identified 26 intersecting genes across purpura, cerebral hemorrhage, and aplastic anemia, with TNF, AKT1, and SRC emerging as key targets. Molecular docking predicted stable binding of gymnoside I to these proteins, and biolayer interferometry confirmed direct interactions, particularly with TNF. Conclusion Gymnoside I exerts multi-target modulation of coagulation and inflammatory pathways, supporting the concept of “treating different diseases with the same approach.” These findings provide mechanistic insight into its pharmacological activity and highlight its potential for further development in hemorrhagic disease therapy.
Fu et al. (2026) studied this question.