Evidence map›Paper›PMID 40159976›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2025

[Protein C activator derived from snake venom protects human umbilical vein endothelial cells against hypoxia-reoxygenation injury by suppressing ROS

Ming Liao, Wenhua Zhong, Ran Zhang, Juan Liang, Wentaorui Xu, Wenjun Wan, Chao Li Shu Wu, 曙 李

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Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

8 authors.

Ming LiaoDepartment of Pathophysiology, Wannan Medical College, Wuhu 241002, China.
Wenhua ZhongDepartment of Pathophysiology, Wannan Medical College, Wuhu 241002, China.
Ran ZhangDepartment of Pathophysiology, Wannan Medical College, Wuhu 241002, China.
Juan LiangDepartment of Pathophysiology, Wannan Medical College, Wuhu 241002, China.
Wentaorui XuDepartment of Pathophysiology, Wannan Medical College, Wuhu 241002, China.
Wenjun WanDepartment of Pathophysiology, Wannan Medical College, Wuhu 241002, China.
Chao Li Shu WuDepartment of Pathophysiology, Wannan Medical College, Wuhu 241002, China.
曙 李Department of Pathophysiology, Wannan Medical College, Wuhu 241002, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate the antioxidative mechanism of snake venom-derived protein C activator (PCA) in mitigating vascular endothelial cell injury.

methodsHuman umbilical vein endothelial cells (HUVECs) were cultured in DMEM containing 1.0 g/L D-glucose and exposed to hypoxia (1% O

resultsIn the OGD/R cell model, PCA treatment significantly upregulated HIF-1α, BNIP3 and Beclin-1 expressions and reduced ROS production. The effects of PCA were obviously attenuated by co-treatment with 2-ME2 but augmented by treatment with DMOG (a HIF-1α stabilizer). In the cell model with BNIP3 knockdown, PCA treatment increased BNIP3 expression and decreased ROS production without causing significant changes in HIF-1α expression. Compared with HUVECs with PCA treatment only, the cells with BNIP3 knockdown prior to PCA treatment showed significantly lower Beclin-1 expression and higher ROS levels.

conclusionsSnake venom PCA alleviates OGD/R-induced endothelial cell injury by upregulating HIF-1α/BNIP3 signaling to suppress ROS generation, suggesting its potential as a therapeutic agent against oxidative stress in vascular pathologies.

Indexed as

Human Umbilical Vein Endothelial CellsHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsProto-Oncogene ProteinsReactive Oxygen SpeciesSnake VenomsBeclin-1Cell HypoxiaCells, CulturedHumansUp-RegulationBeclin-1BNIP3 protein, humanHIF1A protein, humanHypoxia-Inducible Factor 1, alpha SubunitMembrane ProteinsProto-Oncogene ProteinsReactive Oxygen SpeciesSnake Venomshypoxia-inducible factor-1αmitochondrial autophagyoxygen-glucose deprivation/reoxygenationprotein C activator

Identifiers

PMID40159976
PMCPMC11955880

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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.