ArticleExperimental and therapeutic medicine2022
Effects and mechanisms of CTRP3 overexpression in secondary brain injury following intracerebral hemorrhage in rats.
Article in Experimental and therapeutic medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
- CTRP family in diseases associated with inflammation and metabolism: molecular mechanisms and clinical implication.Acta pharmacologica Sinica · 2023Review
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8 authors at 1 institution in 1 country.
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Abstract
C1q/TNF-related protein-3 (CTRP3) is a novel adipokine that serves an important role in oxidative stress, anti-apoptosis, anti-inflammation and immune regulation. The aim of the present study was to investigate the protective role of CTRP3 against intracerebral hemorrhage (ICH)-induced brain injury. A model of autologous arterial blood-induced ICH was constructed in rats. Intracerebral infusion of a lentivirus carrying the CTRP3 gene was used to induce CTRP3 overexpression in the brain. The effects and mechanisms of CTRP3 overexpression on brain injury were investigated by detecting brain edema, blood-brain barrier (BBB) integrity, neurological function and inflammatory-associated factors 3 days after ICH. The present results demonstrated that CTRP3 overexpression ameliorated ICH-induced neurological dysfunction, decreased brain edema, maintained BBB integrity and attenuated inflammation. The protective effect of CTRP3 overexpression was associated with increased activation of silent information regulator 1 (SIRT1). In conclusion, the present study demonstrated that CTRP3 overexpression protected against ICH-induced brain injury in rats, potentially via activating the SIRT1 signaling pathway.
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