[Effect of esomeprazole upon intestinal mucosal damage following traumatic brain injury in rats].
OBJECTIVE
To explore the protective effect of esomeprazole upon stress-related intestinal mucosal damage following traumatic brain injury (TBI) in rats.


METHODS
Male Wistar rats were randomly divided into three groups: groups A and B served as TBI models and group C was designated as a normal control (shame operation). In group B rats were treated subcutaneously with esomeprazole prior to TBI while groups A and C rats were treated with an equivalent amount of normal saline. During the observation period, the morphological changes of brain tissue and intestinal mucosa were observed. And the intestinal mucosal permeability to fluorescein isothiocyanate (FITC)-labeled dextran and diamine oxidase (DAO) activity were assessed. The activities of superoxide dismutase (SOD), myeloperoxidase (MPO) and the levels of malondialdehyde (MDA), reduced glutathione (GSH) and hydroxyl radical (OH(*)) were measured.


RESULTS
(1) During the observation period of TBI, the intestinal mucosal was damaged, but there was improvement in group PPI. (2) FITC-dextran leakage increased after TBI and peaked at 24 h (P < 0.01); its level of (3720 +/- 401) ng/ml in group PPI was lower than that in group TBI (5230 +/- 489) ng/ml (P < 0.05). (3) The DAO activity in mucosa decreased and the decline was the greatest at 24 h (P < 0.05), its level of (0.44 +/- 0.11) ng/ml in group PPI at 24 h was higher than that in group TBI (0.31 +/- 0.07) ng/ml (P < 0.05); while the DAO activity in serum increased significantly. (4) The activity of SOD and the level of GSH in intestinal mucosal started to decrease at 3 h and the decline was the greatest at 24 h (P < 0.05), their levels were (10.2 +/- 2.8) U/mgprot and (140 +/- 46) mg/gprot respectively in group TBI, a remarkable drop in comparison with those of PPI group (13.0 +/- 2.4) U/mgprot and (208 +/- 48) U/gprot (P < 0.05). (5) The levels of OH(.), MDA and MPO in intestinal mucosal increased and peaked at 24 h (P < 0.05), the respective levels in group PPI (108 +/- 8), (6.2 +/- 0.6) and (1.53 +/- 0.52) U/mgprot and those in the TBI group (150 +/- 8), (7.7 +/- 0.9), (1.93 +/- 0.53) U/mgprot, demonstrated that there was a remarkable rise (P < 0.05).


CONCLUSIONS
Traumatic brain injury may lead to stress-related intestinal mucosal damage. Oxygen free radicals play an important role in intestinal mucosal barrier damage. Esomeprazole attenuates the damage of intestinal mucosal barrier by antioxidant effect and inhibiting the activity of neutrophil.
Lü
Dong
D
Department of Gastroenterology, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.
Cui
Pei-lin
PL
Yang
Zhao-xu
ZX
D000818:Animals; D001930:Brain Injuries / Q000378:metabolism* / Q000473:pathology; D064098:Esomeprazole / Q000494:pharmacology*; D005609:Free Radicals / Q000378:metabolism; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000473:pathology; D007422:Intestines; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism
D005609:Free Radicals; D017382:Reactive Oxygen Species; D064098:Esomeprazole