Astilbin ameliorates intracerebral hemorrhage-induced secondary brain injury by upregulating Treg cells in mice

Abstract

Background: Intracerebral Hemorrhage (ICH) is a common acute fatal cerebrovascular disease in surgery. Astilbin, a flavonoid extracted from various plants, has been studied for its excellent anti-inflammatory action. The present study aims to investigate the efficacy and mechanism of astilbin against ICH in mice.

Methods: The ICH in C57BL/6 mice was induced with classical autologous blood injection. We conducted behavioral tests, Perls' staining, Nissl staining, TUNEL staining, Evans blue dye extravasation, water content, Enzyme-linked immunosorbent assay (ELISA), immunofluorescence staining to access the anti-inflammatory function of astilbin.

Results: Astilbin demonstrates a capacity to ameliorate neurofunctional impairments induced by ICH in mice. It effectively reduces iron deposition and neuronal death in the peri-hematoma tissue. Astilbin alleviates cerebral edema and mitigates blood-brain barrier (BBB) damage caused by ICH. Furthermore, astilbin promotes the secretion of chemotactic and anti-inflammatory factors post-ICH, including CCL1, CCL20, IL-10, IL-35, and TGFβ. Notably, astilbin facilitates the accumulation of Treg cells in the brain tissue surrounding the hematoma after ICH.

Conclusion: Astilbin facilitates the enrichment of Treg cells in the brain tissue around the hematoma, thereby alleviating secondary brain injury (SBI) following ICH and improving the overall prognosis of ICH. These findings suggest its potential candidacy as a therapeutic intervention for mitigating the consequences of intracerebral hemorrhage.

Keywords: Anti-inflammation; Astilbin; Intracerebral hemorrhage; Secondary brain injury; Treg.