中国免疫学杂志
中國免疫學雜誌
중국면역학잡지
CHINESE JOURNAL OF IMMUNOLOGY
2014年
6期
726-730
,共5页
郑桐%杨天飞%车筑平%谭庆华
鄭桐%楊天飛%車築平%譚慶華
정동%양천비%차축평%담경화
阿司匹林%肠黏膜屏障%NSAIDs性肠病%前列腺素E2%生长抑素%表皮生长因子受体
阿司匹林%腸黏膜屏障%NSAIDs性腸病%前列腺素E2%生長抑素%錶皮生長因子受體
아사필림%장점막병장%NSAIDs성장병%전렬선소E2%생장억소%표피생장인자수체
Aspirin%Intestinal-mucous-barrier%NSAIDs-interopathy%Prostaglandin-E2%Somatostatin%Epidermal-growth-factor-receptor
目的：探讨非甾体类消炎药（ Non-steroid anti-inflammatory drugs ，NSAIDs）阿司匹林注射液对SD大鼠回肠生长抑素（Somatostatin，SST）、表皮生长因子受体（Epidermal growth factor receptor ，EGFR）、前列腺素E2（Prostaglandin E2，PGE2）及黏液影响。方法：取32只SD大鼠随机分为灌胃组、灌肠组、腹腔注射组及空白对照组四组，每组8只。对回肠黏膜损伤进行评分，阿利辛蓝染色显示其黏液的分布并测定阳性面积及积分光密度（ Integrated option density ，IOD）值；ELISA检测各组回肠组织SST、EGFR、PGE2水平；免疫组化检测各组回肠组织SST、EGFR、PGE2的分布，图像分析软件测定IOD值。结果：阿司匹林治疗组肠黏膜损伤指数比正常对照组高（ P＜0.05），两两比较黏膜损伤评分无差别；其黏液的面积和IOD值均比正常对照组低（ P＜0.05），其中腹腔注射组的面积（602.17±158.03）及IOD值（249.54±113.19）最低（ P＜0.05）。四组间的SST、EGFR浓度、IOD值差异无统计学意义，四组间PGE2浓度、IOD值相比较，空白对照组最高（ P＜0.05），三组阿司匹林组间两两比较其水平没有差异。结论：阿司匹林在不同给药途径下，2周均可引起大鼠小肠黏膜的损伤。这种损伤中，小肠黏膜的完整性破坏和黏膜黏液的分泌受到了明显影响，而腹腔注射给药对小肠黏膜黏液的合成和分泌影响最大，可能这些改变与PGE2的降低有关。无明确结果表明SST和EGFR参与了NSAIDs性肠病的病理生理过程。
目的：探討非甾體類消炎藥（ Non-steroid anti-inflammatory drugs ，NSAIDs）阿司匹林註射液對SD大鼠迴腸生長抑素（Somatostatin，SST）、錶皮生長因子受體（Epidermal growth factor receptor ，EGFR）、前列腺素E2（Prostaglandin E2，PGE2）及黏液影響。方法：取32隻SD大鼠隨機分為灌胃組、灌腸組、腹腔註射組及空白對照組四組，每組8隻。對迴腸黏膜損傷進行評分，阿利辛藍染色顯示其黏液的分佈併測定暘性麵積及積分光密度（ Integrated option density ，IOD）值；ELISA檢測各組迴腸組織SST、EGFR、PGE2水平；免疫組化檢測各組迴腸組織SST、EGFR、PGE2的分佈，圖像分析軟件測定IOD值。結果：阿司匹林治療組腸黏膜損傷指數比正常對照組高（ P＜0.05），兩兩比較黏膜損傷評分無差彆；其黏液的麵積和IOD值均比正常對照組低（ P＜0.05），其中腹腔註射組的麵積（602.17±158.03）及IOD值（249.54±113.19）最低（ P＜0.05）。四組間的SST、EGFR濃度、IOD值差異無統計學意義，四組間PGE2濃度、IOD值相比較，空白對照組最高（ P＜0.05），三組阿司匹林組間兩兩比較其水平沒有差異。結論：阿司匹林在不同給藥途徑下，2週均可引起大鼠小腸黏膜的損傷。這種損傷中，小腸黏膜的完整性破壞和黏膜黏液的分泌受到瞭明顯影響，而腹腔註射給藥對小腸黏膜黏液的閤成和分泌影響最大，可能這些改變與PGE2的降低有關。無明確結果錶明SST和EGFR參與瞭NSAIDs性腸病的病理生理過程。
목적：탐토비치체류소염약（ Non-steroid anti-inflammatory drugs ，NSAIDs）아사필림주사액대SD대서회장생장억소（Somatostatin，SST）、표피생장인자수체（Epidermal growth factor receptor ，EGFR）、전렬선소E2（Prostaglandin E2，PGE2）급점액영향。방법：취32지SD대서수궤분위관위조、관장조、복강주사조급공백대조조사조，매조8지。대회장점막손상진행평분，아리신람염색현시기점액적분포병측정양성면적급적분광밀도（ Integrated option density ，IOD）치；ELISA검측각조회장조직SST、EGFR、PGE2수평；면역조화검측각조회장조직SST、EGFR、PGE2적분포，도상분석연건측정IOD치。결과：아사필림치료조장점막손상지수비정상대조조고（ P＜0.05），량량비교점막손상평분무차별；기점액적면적화IOD치균비정상대조조저（ P＜0.05），기중복강주사조적면적（602.17±158.03）급IOD치（249.54±113.19）최저（ P＜0.05）。사조간적SST、EGFR농도、IOD치차이무통계학의의，사조간PGE2농도、IOD치상비교，공백대조조최고（ P＜0.05），삼조아사필림조간량량비교기수평몰유차이。결론：아사필림재불동급약도경하，2주균가인기대서소장점막적손상。저충손상중，소장점막적완정성파배화점막점액적분비수도료명현영향，이복강주사급약대소장점막점액적합성화분비영향최대，가능저사개변여PGE2적강저유관。무명학결과표명SST화EGFR삼여료NSAIDs성장병적병리생리과정。
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 .
