Journal of advanced research · 2025
A mouse model of sepsis-associated DIC induced by Kappa-carrageenan and Lipopolysaccharides: Establishment and characteristics.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Tang Ping, Huang Boning, Ou Qianqing, Liu Fangle, Lin Liuqing, Zheng Yuying, Xie Huiyi, Yang Xinrong, Zhang Xiubing, Kuang Zhongsheng, Xie Yuhui, Sun Jingjing, Lin Bingqing, Li Jun, Lin Baoqin
Аннотация
BACKGROUND: No animal models fully replicate the pathogenesis and clinical features of sepsis-associated disseminated intravascular coagulation (DIC), which hinders mechanistic understanding and treatment development. Kappa-carrageenan (KCG) and lipopolysaccharides (LPS) induce thrombosis and systemic inflammation in mice, respectively. The combination of LPS and KCG provides a promising method for establishing a mouse model of sepsis-associated DIC.
OBJECTIVE: This study aimed to establish a standardized mouse model of sepsis-associated DIC using KCG and LPS.
METHODS: Kunming (KM) mice were intraperitoneally injected with KCG (25-200 mg/kg) alone or in combination with LPS (50-1250 μg/kg) to determine optimal dose. The effects of ambient temperature, gender and mouse strains on the mouse model were evaluated. Time-dependent changes in the model were examined.
RESULTS: The combined injection of KCG (100 mg/kg) and LPS (50 μg/kg) effectively induced tail thrombosis and prolonged activated partial thromboplastin time. Mice housed at 16 ± 1℃ exhibited more severe thrombosis and hypocoagulability than those at 24 ± 1℃. Male and female mice exhibited similar responses. Time-course analysis revealed inflammation and blood hypocoagulability beginning from 1.5 to 24 h, with fibrinolysis inhibition occurring within 1 h. Tail thrombosis and auricle petechial developed at 3 and 6 h, respectively, and stabilized by 12 h. Thrombi in the tail, lung and liver along with organ dysfunction were obeserved at 12 h. KM and BALB/c mice exhibited longer tail thrombi than Institute of Cancer Research (ICR) mice. KM mice showed more severe blood hypocoagulability than ICR and BALB/c mice.
CONCLUSIONS: This study establishes a standardized mouse model of sepsis-associated DIC using KCG and LPS, which more accurately replicates the key clinical and pathological characteristics of sepsis-associated DIC compared to existing models. This model serves as a novelty and valuable tool for investigating the mechanisms of sepsis-associated DIC and therapeutic evaluation.
OBJECTIVE: This study aimed to establish a standardized mouse model of sepsis-associated DIC using KCG and LPS.
METHODS: Kunming (KM) mice were intraperitoneally injected with KCG (25-200 mg/kg) alone or in combination with LPS (50-1250 μg/kg) to determine optimal dose. The effects of ambient temperature, gender and mouse strains on the mouse model were evaluated. Time-dependent changes in the model were examined.
RESULTS: The combined injection of KCG (100 mg/kg) and LPS (50 μg/kg) effectively induced tail thrombosis and prolonged activated partial thromboplastin time. Mice housed at 16 ± 1℃ exhibited more severe thrombosis and hypocoagulability than those at 24 ± 1℃. Male and female mice exhibited similar responses. Time-course analysis revealed inflammation and blood hypocoagulability beginning from 1.5 to 24 h, with fibrinolysis inhibition occurring within 1 h. Tail thrombosis and auricle petechial developed at 3 and 6 h, respectively, and stabilized by 12 h. Thrombi in the tail, lung and liver along with organ dysfunction were obeserved at 12 h. KM and BALB/c mice exhibited longer tail thrombi than Institute of Cancer Research (ICR) mice. KM mice showed more severe blood hypocoagulability than ICR and BALB/c mice.
CONCLUSIONS: This study establishes a standardized mouse model of sepsis-associated DIC using KCG and LPS, which more accurately replicates the key clinical and pathological characteristics of sepsis-associated DIC compared to existing models. This model serves as a novelty and valuable tool for investigating the mechanisms of sepsis-associated DIC and therapeutic evaluation.