Preliminary study on effect of aspirin against endogenous protective factors of intestinal mucosa in SD rats
10.3969/j.issn.1000-484X.2014.06.002
- VernacularTitle:阿司匹林对SD大鼠小肠内源性保护因素影响的初探
- Author:
Tong ZHENG
;
Tianfei YANG
;
Zhuping CHE
;
Qinghua TAN
- Publication Type:Journal Article
- Keywords:
Aspirin;
Intestinal-mucous-barrier;
NSAIDs-interopathy;
Prostaglandin-E2;
Somatostatin;
Epidermal-growth-factor-receptor
- From:
Chinese Journal of Immunology
2014;(6):726-730
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the changes of somatostatin ,epidermal growth factor receptor ,prostaglandin E2 and mucus of ileum in SD rats injected aspirin.Methods:32 SD rats were randomly divided into 4 groups:oral intake group ,coloclyster group ,in-traperitoneal injection group and normal control group.Ileal tissue sections were stained by Alcian blue.The positive area and IOD of Alcian blue was counted by image analysis in each group.The concentration of SST ,EGFR and PGE2 were detected by ELISA immuno-histochemistry ,and the IOD of each index was measured by image analysis in each group.Results:The score of ileum mucosal injury were highest in aspirin treatment groups ( P<0.05 ) ,but the score was no difference among aspirin treatment groups.The area and IOD of mucus in aspirin treatment groups were less than normal control group .The Area ( 602.17 ±158.03 ) and level of IOD ( 249.54 ± 113.19) in intraperitoneal injection group was the lowest (P<0.05).There were no differences of level of SST ,EGFR was observed among all groups .The concentration and IOD of PGE2 in normal control group was the highest (P<0.05).However,his discrepancy was not obvious among three groups of aspirin.Conclusion: Aspirin, in the four routes of administration , can cause damage to the mucosa of the rat small intestine in two weeks.The integrity of the small intestinal mucosa and mucus secretion were damaged significantly ,and it was the worst in intraperitoneal injection group.These changes might be correlated with the reduction of PGE 2.No clear results showed that the SST and EGFR were involved in the pathophysiology of the NSAIDs .
