中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2015年
5期
759-765
,共7页
实验动物%消化系统损伤模型%急性胰腺炎%N-乙酰半胱氨酸%牛黄胆酸盐%炎症因子%血清淀粉酶%核因子κB%炎症反应
實驗動物%消化繫統損傷模型%急性胰腺炎%N-乙酰半胱氨痠%牛黃膽痠鹽%炎癥因子%血清澱粉酶%覈因子κB%炎癥反應
실험동물%소화계통손상모형%급성이선염%N-을선반광안산%우황담산염%염증인자%혈청정분매%핵인자κB%염증반응
Pancreatitis%Inflammation%Interleukins%Pancreatic Islet
背景：急性胰腺炎是由胰腺腺泡细胞损伤介导的常见炎性疾病，白细胞浸润是其主要的发病特征。近来发现N-乙酰半胱氨酸能够控制白细胞游走并在一些严重的炎症疾病中发挥调节炎症反应的作用。
<br> 目的：观察N-乙酰半胱氨酸在体内对牛黄胆酸盐诱导的急性胰腺炎大鼠模型的保护作用。
<br> 方法：90只SD大鼠随机等分为正常对照组、急性胰腺炎组和N-乙酰半胱氨酸组，后2组以十二指肠大乳头逆行注射牛黄胆酸盐制备急性大鼠胰腺炎模型。N-乙酰半胱氨酸组大鼠由尾静脉给予N-乙酰半胱氨酸治疗。结果与结论：急性胰腺炎模型诱导后大鼠血浆淀粉酶活性较正常对照组大鼠显著升高(P<0.05)。急性胰腺炎组白细胞介素1β，6，10和肿瘤坏死因子α表达水平明显高于正常对照组(P<0.05)。免疫荧光化学显示N-乙酰半胱氨酸主要表达在胰岛细胞上，急性胰腺炎组织 N-乙酰半胱氨酸的表达从 mRNA 水平到蛋白水平都明显低于正常组织。N-乙酰半胱氨酸治疗显著降低了大鼠血清淀粉酶水平，髓过氧化物酶活性以及促炎性细胞因子产物生产和胰腺及肺组织损伤，但N-乙酰半胱氨酸治疗并没有明显抑制胰腺组织核因子κB的激活。提示N-乙酰半胱氨酸能改善急性胰腺炎大鼠胰腺和肺脏的组织损伤，并发挥抗炎症的作用。
揹景：急性胰腺炎是由胰腺腺泡細胞損傷介導的常見炎性疾病，白細胞浸潤是其主要的髮病特徵。近來髮現N-乙酰半胱氨痠能夠控製白細胞遊走併在一些嚴重的炎癥疾病中髮揮調節炎癥反應的作用。
<br> 目的：觀察N-乙酰半胱氨痠在體內對牛黃膽痠鹽誘導的急性胰腺炎大鼠模型的保護作用。
<br> 方法：90隻SD大鼠隨機等分為正常對照組、急性胰腺炎組和N-乙酰半胱氨痠組，後2組以十二指腸大乳頭逆行註射牛黃膽痠鹽製備急性大鼠胰腺炎模型。N-乙酰半胱氨痠組大鼠由尾靜脈給予N-乙酰半胱氨痠治療。結果與結論：急性胰腺炎模型誘導後大鼠血漿澱粉酶活性較正常對照組大鼠顯著升高(P<0.05)。急性胰腺炎組白細胞介素1β，6，10和腫瘤壞死因子α錶達水平明顯高于正常對照組(P<0.05)。免疫熒光化學顯示N-乙酰半胱氨痠主要錶達在胰島細胞上，急性胰腺炎組織 N-乙酰半胱氨痠的錶達從 mRNA 水平到蛋白水平都明顯低于正常組織。N-乙酰半胱氨痠治療顯著降低瞭大鼠血清澱粉酶水平，髓過氧化物酶活性以及促炎性細胞因子產物生產和胰腺及肺組織損傷，但N-乙酰半胱氨痠治療併沒有明顯抑製胰腺組織覈因子κB的激活。提示N-乙酰半胱氨痠能改善急性胰腺炎大鼠胰腺和肺髒的組織損傷，併髮揮抗炎癥的作用。
배경：급성이선염시유이선선포세포손상개도적상견염성질병，백세포침윤시기주요적발병특정。근래발현N-을선반광안산능구공제백세포유주병재일사엄중적염증질병중발휘조절염증반응적작용。
<br> 목적：관찰N-을선반광안산재체내대우황담산염유도적급성이선염대서모형적보호작용。
<br> 방법：90지SD대서수궤등분위정상대조조、급성이선염조화N-을선반광안산조，후2조이십이지장대유두역행주사우황담산염제비급성대서이선염모형。N-을선반광안산조대서유미정맥급여N-을선반광안산치료。결과여결론：급성이선염모형유도후대서혈장정분매활성교정상대조조대서현저승고(P<0.05)。급성이선염조백세포개소1β，6，10화종류배사인자α표체수평명현고우정상대조조(P<0.05)。면역형광화학현시N-을선반광안산주요표체재이도세포상，급성이선염조직 N-을선반광안산적표체종 mRNA 수평도단백수평도명현저우정상조직。N-을선반광안산치료현저강저료대서혈청정분매수평，수과양화물매활성이급촉염성세포인자산물생산화이선급폐조직손상，단N-을선반광안산치료병몰유명현억제이선조직핵인자κB적격활。제시N-을선반광안산능개선급성이선염대서이선화폐장적조직손상，병발휘항염증적작용。
BACKGROUND:Acute pancreatitis is a common inflammatory disease mediated by pancreatic acinar cel s injury, and is mainly characterized by leukocyte infiltration. N-acetylcysteine can control leukocyte migration and regulate inflammation in some serious inflammatory diseases. OBJECTIVE:To investigate the protective effects of N-acetylcysteine in rat model of acute pancreatitis caused by sodium taurocholate. METHODS:Ninety Sprague-Dawley rats were randomly divided into three groups:normal control group, acute pancreatitis group and N-acetylcysteine group. Except normal control group, acute pancreatitis model was established in the other two groups by retrograde injection of sodium taurocholate into major duodenal papil a. Rats in the N-acetylcysteine group were treated with N-acetylcysteine intravenously through the tail vein. RESULTS AND CONCLUSION:After acute pancreatitis model was established, plasma amylase levels in the models were significantly higher than that in the normal control rats (P<0.05). Interleukin-1β,-6,-10, and tumor necrosis factorαexpression levels were also obviously higher than that in the normal control rats (P<0.05). Immunohistochemical staining demonstrated that N-acetylcysteine was mainly expressed in the islet cel s, and the pancreatic expression of N-acetylcysteine was down-regulated at both the mRNA and protein levels during the course of acute pancreatitis. N-acetylcysteine administration significantly reduced plasma amylase levels, myeloperoxidase activity, pro-inflammatory cytokine production, and pancreas and lung tissue damages. Furthermore, N-acetylcysteine administration did not cause significant inhibition of nuclear factor-κB activation in the pancreas. N-acetylcysteine is capable of improving damage of pancreas and lung, and exerting anti-inflammatory effects in rats with severe acute pancreatitis.
