The Effects of Female Sex Steroids on Gastric Secretory Responses of Rat Following Traumatic Brain Injury

• Main Authors: Zakieh Keshavarzi, Mohammad Khaksari Hadad, Mohammad Javad Zahedi, Abbas Bahrami
• Format: Article
• Language: English
• Published: Mashhad University of Medical Sciences 2011-05-01
• Series: Iranian Journal of Basic Medical Sciences
• Subjects: Brain injury; Estrogen; Gastric acid; Pepsin; Progesterone
• Online Access: http://www.mums.ac.ir/shares/basic_medical/basicmedjou/2011/may/a6.pdf

AbstractObjective(s)Gastric ulceration is induced by various forms of stress like surgery, ischemia and trauma. The female sex has more resistance to stress and the gastrointestinal lesions happen fewer than male sex. The purpose of this study was to evaluate the role of estradiol and progesterone on the gastric acid and pepsin levels following traumatic brain injury (TBI) induction.Materials and MethodsDiffuse TBI was induced by Marmarou method in female rats. Rats randomly assigned into 9 groups: intact, OVX (ovarectomized rat), Sham+OVX, TBI (intact rats under TBI), TBI+OVX (ovarectomized rats under TBI) and treated OVX rats with vehicle (sesame oil), E2 (estradiol), P4 (progesterone) or E2+P4 combination. The acid content and pepsin levels of each gastric washout sample were measured 5 days after the TBI induction.ResultsThere was no significant difference in gastric acid output between groups either after TBI induction or after treatment with E2 or P4 or E2+P4. Gastric pepsin levels were increased in Sham+OVX, TBI (P< 0.001) and TBI+OVX (P< 0.05) compared to intact group. Gastric pepsin levels were significantly lower in E2 and E2+ P4 treated rats than vehicle treated group (P< 0.01). P4 treatment increased gastric pepsin level compared to TBI+OVX group (P< 0.05) and this increment was higher than rats that were treated with the E2 and E2+P4 (P< 0.01).ConclusionThese results suggest that protective effect of estradiol and E2+P4 combination against mucosal damage after TBI, might be mediated by inhibition of pepsin secretion.