Research Article

Effects of thrombin on the secondary cerebral injury of perihematomal tissues of rats after intracerebral hemorrhage

Published: June 18, 2014
Genet. Mol. Res. 13 (2) : 4617-4626 DOI: https://doi.org/10.4238/2014.June.18.4
Cite this Article:
C.M. Liu, B.Z. Shi, J.S. Zhou (2014). Effects of thrombin on the secondary cerebral injury of perihematomal tissues of rats after intracerebral hemorrhage. Genet. Mol. Res. 13(2): 4617-4626. https://doi.org/10.4238/2014.June.18.4
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Abstract

This study aimed to investigate the effects of thrombin released in hematoma after intracerebral hemorrhage (ICH) on the cerebral injury of perihematomal tissues and to evaluate the protection effect of hirudin on the cerebral injury after ICH. We used the autologous uncoagulated blood injection method to prepare the ICH rat model, and all rats were randomly divided into a normal group, an ICH group, or a hirudin group. At different time points, rat heads were cut to harvest brain sections. Immunohistochemical staining, histochemical staining, and hematoxylin and eosin staining were conducted for CD34, microglia, and neutrocytes. CD34-positive microvessels were most abundant in brain tissues of the sham-operation group. At 12 h after ICH, CD34 expression reduced and reached the minimum level at 72 h (P < 0.01). At 6 h after ICH, microglia expression was visible and reached a peak at 48 h (P < 0.01). At 12 h after ICH, neutrocyte infiltration was visible and the number was greatest at 48 h (P < 0.01). The early application of hirudin after ICH could significantly reduce microglia and neutrocyte expression and could significantly slow down the CD34 decrease trend (P < 0.01). However, hirudin application in the edematization stage after ICH did not significantly increase CD34- positive microvessel abundance (P > 0.05). A thrombin-mediated inflammatory reaction is involved in the cerebral injury after ICH, and the early application of hirudin has a protective effect.

This study aimed to investigate the effects of thrombin released in hematoma after intracerebral hemorrhage (ICH) on the cerebral injury of perihematomal tissues and to evaluate the protection effect of hirudin on the cerebral injury after ICH. We used the autologous uncoagulated blood injection method to prepare the ICH rat model, and all rats were randomly divided into a normal group, an ICH group, or a hirudin group. At different time points, rat heads were cut to harvest brain sections. Immunohistochemical staining, histochemical staining, and hematoxylin and eosin staining were conducted for CD34, microglia, and neutrocytes. CD34-positive microvessels were most abundant in brain tissues of the sham-operation group. At 12 h after ICH, CD34 expression reduced and reached the minimum level at 72 h (P 0.05). A thrombin-mediated inflammatory reaction is involved in the cerebral injury after ICH, and the early application of hirudin has a protective effect.

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