Evidence map›Paper›PMID 40118341›Full record

ArticleJournal of advanced research2026

A mouse model of sepsis-associated DIC induced by Kappa-carrageenan and Lipopolysaccharides: Establishment and characteristics.

Ping Tang, Boning Huang, Qianqing Ou, Fangle Liu, Liuqing Lin, Yuying Zheng, Huiyi Xie, Xinrong Yang, Xiubing Zhang, Zhongsheng Kuang and 5 more

Abstract read
In one paragraph

Article in Journal of advanced research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

15 authors.

Ping TangThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Boning HuangThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Qianqing OuThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Fangle LiuThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Liuqing LinThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Yuying ZhengThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Huiyi XieThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Xinrong YangThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Xiubing ZhangThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Zhongsheng KuangThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Yuhui XieThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China.
Jingjing SunGreater Bay Area Institute of Precision Medicine (Guangzhou), Guangzhou, Guangdong 511462, China.
Bingqing LinSchool of Mathematical Sciences, Shenzhen University, Shenzhen, Guangdong 518060, China. Electronic address: bqlin@szu.edu.cn.
Jun LiThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China. Electronic address: lijun@gzucm.edu.cn.
Baoqin LinThe First Affiliated Hospital of Guangzhou University of Chinese Medicine, Guangzhou, Guangdong 510405, China; Guangdong Clinical Research Academy of Chinese Medicine, Guangzhou, Guangdong 510405, China. Electronic address: linbqcpu@126.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNo 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.

objectiveThis study aimed to establish a standardized mouse model of sepsis-associated DIC using KCG and LPS.

methodsKunming (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.

resultsThe 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.

conclusionsThis 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.

Indexed as

CarrageenanDisease Models, AnimalDisseminated Intravascular CoagulationLipopolysaccharidesSepsisAnimalsFemaleMaleMiceThrombosisCarrageenanLipopolysaccharidesKappa-carrageenanLPSmouse modelsepsis-associated DIC

Identifiers

PMID40118341
PMCPMC12766204

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LicenceCC BY-NC-ND
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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.