Tumor necrosis factor-α-stimulated gene 6 promotes hematoma clearance after intracerebral hemorrhage in a mouse model.

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

The prognosis for patients who experience intracerebral hemorrhage is poor because of a lack of effective treatments. Tumor necrosis factor-α–stimulated gene 6 (TSG6) is a secreted glycoprotein that exerts anti-inflammatory effects in various inflammatory diseases. We previously showed that adipose-derived stem cells can inhibit inflammation by upregulating TSG6 secretion in an in vitro model of intracerebral hemorrhage. However, the direct effects of TSG6 on hematoma clearance in vivo remain largely unknown. The aim of this study was to determine how TSG6 affects hematoma absorption in mice subjected to intracerebral hemorrhage and to explore the potential underlying mechanisms. We first analyzed the gene profiles of patients with intracerebral hemorrhage from the GEO database and examined changes in TSG6 expression in the brain tissues of mice subjected to intracerebral hemorrhage. We found that TSG6 expression exhibited a transient increase following intracerebral hemorrhage, and that there was a negative correlation between the initial hematoma volume and TSG6 levels. Immunofluorescence analysis showed that TSG6 was primarily expressed in microglia and macrophages. Furthermore, we found that TSG6 promoted functional recovery in mice subjected to intracerebral hemorrhage by accelerating hematoma clearance, reducing the number of apoptotic cells and degenerated neurons, incre

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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