Decreased neutrophil levels in mice with traumatic brain injury after cape administration

Peripheral leukocytes can worsen brain damage due to the release of cytotoxic mediators that interfere the blood brain barrier function. One of the oxidants released by activation leukocyte is hypochlorite acid (HOCl) which is formed through the myeloperoxidase (MPO)-H2O2-Cl^- system. The neuroprotective effects of an experimental anti-inflammatory drug Caffeic Acid Phenethyl Ester (CAPE) tested in a Traumatic brain injury (TBI) model using Myeloperoxidase (MPO) analysis.

This study compares the acute inflammatory response to TBI over time, as measured by MPO activity. Adult Sprague mice were treated for head trauma with marmarou model. At 24 h before trauma, all animals were blood test (n = 10) to examine MPO, then the animal was divided into 2 groups of injured animals treated with CAPE (n = 5), and those not treated with CAPE (n = 5). We used the MPO test to identify the level of polymorphonuclear leukocytes (PMNL) on day 4 and day 7.

Showed an increase in PMNL infiltration in CAPE untreated animals, this change significantly (P < 0.05) decreased at group of animals treated with CAPE. MPO serum activity in the CAPE untreated group vs treated with CAPE on day 4 ± 11920410.076 (Standard deviation {SD} 895355.169) vs 6663184.485 (SD 895355.169) p < 0,05 and on day 7 ± 14223286.992 (SD 802762.401) vs 9284222.028 (SD 953098.093) p < 0,05. These data indicate that MPO activity after TBI increases on day 4 also on day 7 and improves after being treated with CAPE.

CAPE can reduce Neutrophil serum levels there by preventing brain damage in TBI.