European journal of pharmacology · 2025
Tryptanthrin impairs platelet function and thrombus formation by reducing Gp1bα expression.
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Gao Hanchen, Huang Jian, Huang Xin, Lin Xiangjie, Li Xia, Deng Huan, Zhou Yulan, Wu Lanlan, Xi Xiaodong, Jin Jie, Huang Jiansong
Аннотация
BACKGROUND: Tryptanthrin (Couroupitine A) is isolated from indigo-bearing traditional Chinese herbal medicines. It has a broad spectrum of pharmacological and biological activities. However, the potential effects of tryptanthrin on platelet function and thrombus formation remain elusive.
METHODS: Platelets were harvested from C57BL/6 mice and healthy individuals. Following incubation with tryptanthrin, various platelet functions were assessed. Thrombus formation in the presence of tryptanthrin was evaluated both in vitro, using a BioFlux 200 microfluidic system, and in vivo, through FeCl3-induced thrombosis and mouse deep venous thrombosis experiments. The closure times of the tryptanthrin-treated whole blood samples were determined using the PFA-200 system. Platelet proteomics sequencing was conducted to elucidate the underlying mechanisms by which tryptanthrin influences platelet function.
RESULTS: Tryptanthrin inhibited mouse platelet function and impaired carotid artery and deep venous thrombus formation. Tryptanthrin also inhibited human platelet spreading, aggregation and clot retraction. The signaling pathways related to platelet activation, aggregation, hemostasis, and the fibrin clotting cascade were significantly suppressed in platelets treated with tryptanthrin. Notably, the expression of Gp1bα in platelets was diminished by tryptanthrin.
CONCLUSIONS: Tryptanthrin impairs platelet function and thrombus formation.
METHODS: Platelets were harvested from C57BL/6 mice and healthy individuals. Following incubation with tryptanthrin, various platelet functions were assessed. Thrombus formation in the presence of tryptanthrin was evaluated both in vitro, using a BioFlux 200 microfluidic system, and in vivo, through FeCl3-induced thrombosis and mouse deep venous thrombosis experiments. The closure times of the tryptanthrin-treated whole blood samples were determined using the PFA-200 system. Platelet proteomics sequencing was conducted to elucidate the underlying mechanisms by which tryptanthrin influences platelet function.
RESULTS: Tryptanthrin inhibited mouse platelet function and impaired carotid artery and deep venous thrombus formation. Tryptanthrin also inhibited human platelet spreading, aggregation and clot retraction. The signaling pathways related to platelet activation, aggregation, hemostasis, and the fibrin clotting cascade were significantly suppressed in platelets treated with tryptanthrin. Notably, the expression of Gp1bα in platelets was diminished by tryptanthrin.
CONCLUSIONS: Tryptanthrin impairs platelet function and thrombus formation.