Biomedicine & Pharmacotherapy (Jul 2024)

The impact of experimental diabetes on intracerebral haemorrhage. A preclinical study

  • Mari Carmen Gómez-de Frutos,
  • Fernando Laso-García,
  • Iván García-Suárez,
  • Dolores Piniella,
  • Laura Otero-Ortega,
  • Elisa Alonso-López,
  • Javier Pozo-Novoa,
  • Rebeca Gallego-Ruiz,
  • Nerea Díaz-Gamero,
  • Blanca Fuentes,
  • María Alonso de Leciñana,
  • Exuperio Díez-Tejedor,
  • Gerardo Ruiz-Ares,
  • María Gutiérrez-Fernández

Journal volume & issue
Vol. 176
p. 116834

Abstract

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Although diabetes mellitus negatively affects post-ischaemic stroke injury and recovery, its impact on intracerebral haemorrhage (ICH) remains uncertain. This study aimed to investigate the effect of experimental diabetes (ED) on ICH-induced injury and neurological impairment. Sprague-Dawley rats were induced with ED 2 weeks before ICH induction. Animals were randomly assigned to four groups: 1)Healthy; 2)ICH; 3)ED; 4)ED-ICH. ICH and ED-ICH groups showed similar functional assessment. The ED-ICH group exhibited significantly lower haemorrhage volume compared with the ICH group, except at 1 mo. The oedema/ICH volume ratio and cistern displacement ratio were significantly higher in the ED-ICH group. Vascular markers revealed greater expression of α-SMA in the ED groups (ED and ED-ICH) compared with ICH. Conversely, the ICH groups (ED-ICH and ICH) exhibited higher levels of VEGF compared to the healthy and ED groups. An assessment of myelin tract integrity showed an increase in fractional anisotropy in the ED and ED-ICH groups compared with ICH. The ED group showed higher cryomyelin expression than the ED-ICH and ICH groups. Additionally, the ED groups (ED and ED-ICH) displayed higher expression of MOG and Olig-2 than ICH. As for inflammation, MCP-1 levels were significantly lower in the ED-ICH groups compared with the ICH group. Notably, ED did not aggravate the neurological outcome; however, it results in greater ICH-related brain oedema, greater brain structure displacement and lower haemorrhage volume. ED influences the cerebral vascularisation with an increase in vascular thickness, limits the inflammatory response and attenuates the deleterious effect of ICH on white matter integrity.

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