Abstract
Objective To evaluate the effect of ulinastatin on Th1/Th2 cell balance in a rat model of stress-induced gastric ulcer (GU).Methods Twenty-four male SPF Sprague-Dawley rats,aged 6-8 weeks,weighing 180-220 g,were randomly divided into 3 groups (n =8 each) using a random number table:control group (group C),stress-induced GU group (group GU) and ulinastatin group (group U).The rats were subjected to water-immersion and restraint stress for 3.5 h to establish GU model in S and U groups.At 10 min before water-immersion,normal saline 0.4 ml and ulinastatin 100 000 U/kg were injected via the tail vein in GU and U groups,respectively.After GU model was established,the abdomen was opened after anesthesia.The whole stomach was exposed,and the gastric mucosal damage was evaluated under microscope,ulcer index (UI) was recorded,and the pathological changes of the gastric mucous membrane were observed.Spleen samples were obtained to detect T-bet,Gata-3,interferon-γ (IFN-γ),and interleukin-4 (IL-4) mRNA expression by RT-PCR.The ratio of T-bet mRNA expression/Gata-3 mRNA expression (T-bet/Gata-3) was calculated.Results Compared with group C,T-bet mRNA expression was significantly down-regulated,Gata-3 mRNA expression was up-regulated,T-bet/Gata-3 ratio was decreased,UI was increased,and no significant changes were found in IFN-γ and IL-4 mRNA expression in GU group,and UI was increased,and no significant changes were found in the other parameters in group U.Compared with group GU,the ratio of T-bet/Gata-3 was significantly increased,and UI was decreased,and no significant changes were found in T-bet,Gata-3,IFN-γ,IL-4 mRNA expression in group U.The gastric mucosal damage was significantly mitigated in GU group as compared with group U.Conclusion The mechanism by which ulinastatin mitigates stress-induced GU may be related to correction of Th1/Th2 cell imbalance in rats. Key words: Trypsin inhibitors; Stomach ulcer; Stress; T-Lymphocytes, helper-inducer
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.