The expression of Galectins-8 and its effect on neuroinflammation after intracerebral hemorrhage

Abstract

Abstract At present, there is no effective treatment for secondary brain injury caused by spontaneous intracerebral hemorrhage (ICH). This study aims to explore new therapeutic targets after ICH. Galectins-8 is a tandem repeat galectin with a unique preference for α2,3-sialylated glycans, and its expression is ubiquitous. Gal − 8 regulates cytokine production, cell adhesion, apoptosis, chemotaxis, endocytosis, differentiation and migration, including immune cells. We used wild-type(WT)C57BL/6J mice and the mice of Galectins-8 gene knockout to establish intracerebral hemorrhage model by collagenase injection and found that Galectins-8 was highly expressed around the hematoma and in the center site of the hematoma after intracerebral hemorrhage. We also found that inhibiting the expression of Galectins-8 or Galectins-8 gene knockout mice may attenuate secondary brain injury following intracerebral hemorrhage by reducing microglia-induced inflammatory responses. Galecectin-8 knockout mice had significantly reduced expression of inflammatory factors, such as TNF-α(P = 0.0353), MCP-1(P = 0.0469), and HMBG1(P = 0.0466). This is in contrast to previous studies that have suggested Galectins-8 as a neuroprotective factor. From this, we draw a conclusion that Galectins-8 played an crucial role in regulating the inflammatory response during intracerebral hemorrhage. Our study highlights Galectins-8 as a potential therapeutic target to protect the brain against secondary brain damage during intracerebral hemorrhage.