Role of Exogenous Corticotropin-releasing Hormone in Cerebral Infarction-related Gastrointestinal Barrier Dysfunction

  Objective  To explore the role of exogenous corticotropin-releasing hormone (CRH) in cerebral infarction-related gastrointestinal barrier dysfunction.

  Methods  Forty male Wistar rats were randomly divided into pseudo-operation group (group C), cerebral infarction group (group Ⅰ), cerebral infarction + intracerebroventricular CRH antagonist group (group A), and cerebral infarction + intraperitoneal CRH group (group H), 10 rats for each group. Urine samples were collected to determine the levels of 24-hour urine epinephrine, norepinephrine, cortisol, and sucrose. Blood samples were taken 24 hours after establishment of the models to determine the activity of diamine oxidase (DAO) and the concentration of D-lactic acid (D-lac). The stomach was taken to determine gastric Guth score, and the tissues of hypothalamus, stomach, jejunum and colon were all taken to determine tissue CRH protein expression using Western blot.

  Results  The changes of urinary cortisol and catecholamine were nearly the same:these indicators in group Ⅰ and group H were significantly higher than those in group C (P < 0.05);in group A were significantly lower than those in group Ⅰ (P < 0.05), in group H were slightly higher than those in group Ⅰ, but with no significant difference; in group H were significantly higher than those in group A (P < 0.05). The changes of urine sucrose exertion, gastric Guth score, plasma DAO activity, plasma D-lac, as well as hypothalamus and gastrointestinal CRH protein content were nearly the same:these indicators in group Ⅰ were significantly higher than those in group C (P < 0.05);in group A were significantly lower than those in group Ⅰ (P < 0.05), in group H were also significantly lower than in group Ⅰ (P < 0.05);however, there was no significant difference between group A and group H.

  Conclusions  After cerebral infarction, gastrointestinal barrier function is damaged. Central use of CRH blocker can decrease cerebral infarction-related gastrointestinal barrier dysfunction. Peripheral use of exogenous CRH can decrease the expression of CRH protein in the brain and the gastrointestinal tract, and also can decrease cerebral infarction-related gastrointestinal barrier dysfunction.