Literature DB >> 32865657

Galectin-9 Promotes Neuronal Restoration via Binding TLR-4 in a Rat Intracerebral Hemorrhage Model.

Tianyu Liang1, Cheng Ma1, Tianyi Wang1, Ruming Deng1, Jiasheng Ding1, Wenjie Wang1, Zhongmou Xu1, Xiang Li1, Haiying Li1, Qing Sun2, Haitao Shen3, Zhong Wang1, Gang Chen1.   

Abstract

Intracerebral hemorrhage (ICH) is a devastating disease with high rates of mortality and morbidity. Galactose lectin-9 (Gal-9) belongs to the family of β-galactoside-binding lectins, which has been shown to play a vital role in immune tolerance and inflammation. However, the function of Gal-9 in ICH has not been fully studied in details. Several experiments were carried out to explore the role of Gal-9 in the late period of ICH. Primarily, ICH models were established in male adult Sprague Dawley (SD) rats. Next, the relative protein levels of Gal-9 at different time points after ICH were examined and the result showed that the level of Gal-9 increased and peaked at the 7th day after ICH. Then we found that when the content of Gal-9 increased, both the number of M2-type microglia and the corresponding anti-inflammatory factors also increased. Through co-immunoprecipitation (CO-IP) analysis, it was found that Gal-9 combines with Toll-like receptor-4 (TLR-4) during the period of the recovery after ICH. TUNEL staining and Fluoro-Jade B staining (FJB) proved that the amount of cell death decreased with the increase of Gal-9 content. Additionally, several behavioral experiments also demonstrated that when the level of Gal-9 increased, the motor, sensory, learning, and memory abilities of the rats recovered better compared to the ICH group. In short, this study illustrated that Gal-9 takes a crucial role after ICH. Enhancing Gal-9 could alleviate brain injury and promote the recovery of ICH-induced injury, so that Gal-9 may exploit a new pathway for clinical treatment of ICH.

Entities:  

Keywords:  Gal-9; ICH; Microglia; Neuroinflammation; Neuronal restoration; TLR-4

Mesh:

Substances:

Year:  2020        PMID: 32865657     DOI: 10.1007/s12017-020-08611-5

Source DB:  PubMed          Journal:  Neuromolecular Med        ISSN: 1535-1084            Impact factor:   3.843


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