Effect of Oxidative Stress on Intestinal Mucosal Barrier Dysfunction Following Traumatic Brain Injury in Rats
10.3969/j.issn.0253-9896.2009.10.019
- VernacularTitle:氧化应激在创伤性脑损伤后肠黏膜屏障损伤中的作用
- Author:
Dong LV
;
Peilin CUI
;
Zhaoxu YANG
- Publication Type:Journal Article
- Keywords:
oxidative stress;
brain injuries;
intestinal mucosa;
reactive oxygen species;
rats;
Wistar
- From:
Tianjin Medical Journal
2009;37(10):874-877,后插3
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To observe the effect of oxidative stress on intestinal mucosal barrier dysfunction following traumatic brain injury (TBI). Methods: Seventy-two male Wistar rats were randomly divided into three groups, group B and group C served as TBI models, group A was designated as the normal controlgroup(shame operation). In group C rats were treated with dimethyl sulfoxide(DMSO) prior to TBI, while rats in group A and B were treated with equivalent normal saline. During the experiment period, the morphological changes of intestinal mucosa were observed, and the intestinal mucosal permeability was detected by measuring the level of endotoxin, diamine oxidase(DAO). Superoxide dismutase(SOD), malondiadehycle (MDA), myeloperoxidase(MPO) and xanthine oxidase(XOD) activities were also detected. Results: During the observed period, the intestinal mucosal barrier function was damaged and the intestinal mucosal permeability increased. The content of endotoxin in serum significantly increased(P < 0.05). As early as 3 h after TBI, the DAO activity in the serum began to increase obviously. At 24 hafter TBI it increased to the highest level(P < 0.05).In group TBI the activity of SOD in intestinal mucosal decreased significantly(P < 0.01); however the levels of MDA and the activity of MPO increased significantly (P < 0.01), the activity of XOD increased significantly as well, and then decreased after 6 h. When pr-treatment with DMSO, intestinal mucosal damage was improved, the content of endotoxin in serum was reduced (P < 0.05), and the increased DAO activity in the serum were inhibited (P < 0.05). When compared with group TBI, there was an inhibition in the decreased activity of SOD and the increased level of MDA in group DMSO (P < 0.05), but they were still higher than that of control group(P < 0.05). There were no significant differences in the activity of XOD and MPO between group DMSO and group TBI. Conclusion: The structure and function of intestinal mucosal barrier were damaged following TBI. Oxidative stress played an important role in the intestinal mucosal barrier dysfunction following TBI. Both XOD and activated polymorphonuclear neutrophils(PMN) were the major source of oxygen free radicals.
