The effect of alprostadil on perihematomal tissue of experimental intracerebral hemorrhage in rats

Abstract

Objective To investigate the effect of alprostadil on perihematomal tissue of experimental intracerebral hemorrhage (ICH) in rats. Methods The ICH was induced by stereotaxic infusion of autologous arterial blood into the right basal ganglion. Forelimb placing test and corner turn test were used as behavioral tests. The rats were tested at 3, 5, 7 and 14 d after ICH. Nissl staining was performed to observe the neuronal morphological changes in perihematomal tissue. Immunofluorescence staining was used to determine the number and distribution of tumor necrosis factor ⁃ α (TNF ⁃ α) and interleukin⁃6 (IL⁃6) positive cells in perihematomal tissue at 3, 5, 7 and 14 d. Results Alprostadil⁃treated group showed significant improvement in behavioral tests at 5, 7 and 14 d compared with the control group (P < 0.05 or P < 0.01), but there was no significant difference at 3 d (P = 0.788, 1.000). Nissl staining showed that after cerebral hemorrhage there were obvious inflammatory infiltration, tissue necrosis presented as a "compressed zone" in the perihematomal tissue, and cells around the zone were swollen and had no apparent profile. After alprostadil treatment inflammatory cell infiltration and swollen neurons were reduced in different degrees. Along with the duration of treatment, neuron gradually increased in cortical area beside the medial fissure ipsilateral to the hemorrhagic side, and achieved approximately to normal level at the end of the therapy (P = 0.650). TNF ⁃ α and IL ⁃6 positive cells were mainly distributed around the hematoma, while there were few positive cells at the distal and contralateral site. After administration of alprostadil TNF⁃α positive cells decreased and IL⁃6 positive cells increased in perihematomal region, and all nearly reached to normal level as the control group at 7 d (P = 0.035, 0.023) and 14 d (P = 0.024, 0.020). Conclusion Alprostadil can improve neurological function of cerebral hemorrhagic rats. The mechanisms may be related to the suppression of acute inflammation and relief of secondary neuron injury around hematomal tissue.

DOI：10.3969/j.issn.1672-6731.2011.03.017