中华实验和临床病毒学杂志
中華實驗和臨床病毒學雜誌
중화실험화림상병독학잡지
CHINESE JOURNAL OF EXPERIMENTAL AND CLINICAL VIROLOGY
2009年
1期
53-55
,共3页
王辉%宋晨昭%孟庆华%任翊%张汾燕%赵敬敬
王輝%宋晨昭%孟慶華%任翊%張汾燕%趙敬敬
왕휘%송신소%맹경화%임익%장분연%조경경
谷氨酰胺%急性肝损伤%肠黏膜
穀氨酰胺%急性肝損傷%腸黏膜
곡안선알%급성간손상%장점막
Ghtamine%Acute liver injury%Intestinal mocosa
目的 探讨谷氨酰胺(glutamine,GLN)对急性肝损伤大鼠肠黏膜屏障的作用.方法 61只清洁级Wistar大鼠随机分为3组:对照组、模型组、GLN干预组.采用脂多糖(lipopolysaccharide,LPS)和D-半乳糖胺(D-galactosamine,D-Gal)腹腔注射法建立急性肝损伤大鼠模型.检测血清丙氨酸转氨酶(ALT)、天冬氨酸转氨酶(AST)和总胆红素(TBiL)水平;光镜下及电镜下观察大鼠肝脏及肠道病理学改变;末端脱氧核苷酸转移酶(TdT)介导的缺口末端标记技术(TUNEL)检测细胞凋亡;高压液相离子色谱仪(HPLC-PED)检测大鼠肠黏膜通透性的改变.结果 模型组及GLN干预组大鼠死亡率差异无统计学意义(P>0.05);模型组及GLN干预组大鼠血清ALT、AST和TBIL水平差异无统计学意义(P>0.05);三组肠黏膜通透性差异无统计学意义(P>0.05);光镜下GLN干预组与模型组大鼠肝脏损伤程度差异无统计学意义;肠道未见明显病变;透射电镜下模型组和GLN干预组大鼠肝脏和肠道出现线粒体和细胞核等损伤,GLN干预组较模型组大鼠损伤轻;GLN干预组肝脏和肠道的凋亡指数(Apoptosis index,AI)显著低于模型组(P<0.05).结论 脂多糖可以造成D-半乳糖胺致敏大鼠急性肝损伤模型,造模前给予谷胺酰胺干预可能对于改善肝功能,保护肠黏膜的通透性,降低死亡率没有显著性作用.
目的 探討穀氨酰胺(glutamine,GLN)對急性肝損傷大鼠腸黏膜屏障的作用.方法 61隻清潔級Wistar大鼠隨機分為3組:對照組、模型組、GLN榦預組.採用脂多糖(lipopolysaccharide,LPS)和D-半乳糖胺(D-galactosamine,D-Gal)腹腔註射法建立急性肝損傷大鼠模型.檢測血清丙氨痠轉氨酶(ALT)、天鼕氨痠轉氨酶(AST)和總膽紅素(TBiL)水平;光鏡下及電鏡下觀察大鼠肝髒及腸道病理學改變;末耑脫氧覈苷痠轉移酶(TdT)介導的缺口末耑標記技術(TUNEL)檢測細胞凋亡;高壓液相離子色譜儀(HPLC-PED)檢測大鼠腸黏膜通透性的改變.結果 模型組及GLN榦預組大鼠死亡率差異無統計學意義(P>0.05);模型組及GLN榦預組大鼠血清ALT、AST和TBIL水平差異無統計學意義(P>0.05);三組腸黏膜通透性差異無統計學意義(P>0.05);光鏡下GLN榦預組與模型組大鼠肝髒損傷程度差異無統計學意義;腸道未見明顯病變;透射電鏡下模型組和GLN榦預組大鼠肝髒和腸道齣現線粒體和細胞覈等損傷,GLN榦預組較模型組大鼠損傷輕;GLN榦預組肝髒和腸道的凋亡指數(Apoptosis index,AI)顯著低于模型組(P<0.05).結論 脂多糖可以造成D-半乳糖胺緻敏大鼠急性肝損傷模型,造模前給予穀胺酰胺榦預可能對于改善肝功能,保護腸黏膜的通透性,降低死亡率沒有顯著性作用.
목적 탐토곡안선알(glutamine,GLN)대급성간손상대서장점막병장적작용.방법 61지청길급Wistar대서수궤분위3조:대조조、모형조、GLN간예조.채용지다당(lipopolysaccharide,LPS)화D-반유당알(D-galactosamine,D-Gal)복강주사법건립급성간손상대서모형.검측혈청병안산전안매(ALT)、천동안산전안매(AST)화총담홍소(TBiL)수평;광경하급전경하관찰대서간장급장도병이학개변;말단탈양핵감산전이매(TdT)개도적결구말단표기기술(TUNEL)검측세포조망;고압액상리자색보의(HPLC-PED)검측대서장점막통투성적개변.결과 모형조급GLN간예조대서사망솔차이무통계학의의(P>0.05);모형조급GLN간예조대서혈청ALT、AST화TBIL수평차이무통계학의의(P>0.05);삼조장점막통투성차이무통계학의의(P>0.05);광경하GLN간예조여모형조대서간장손상정도차이무통계학의의;장도미견명현병변;투사전경하모형조화GLN간예조대서간장화장도출현선립체화세포핵등손상,GLN간예조교모형조대서손상경;GLN간예조간장화장도적조망지수(Apoptosis index,AI)현저저우모형조(P<0.05).결론 지다당가이조성D-반유당알치민대서급성간손상모형,조모전급여곡알선알간예가능대우개선간공능,보호장점막적통투성,강저사망솔몰유현저성작용.
Objective To explore the role of glutamine in LPS and D-Gal induced acute hepatic injury. Methods A total of 61 Wistar rats were randomly divided into three groups:control group, model group and GLN pretreated group.The animal model was established by LPS and D-Gal intraperitoneal injection. GLN at dose of 1 g/kg was intragastrically administrated for 7 d before intraperitoneal injection. To evaluate the hepatic injury, the serum alanine aminotransferase(ALT), aspartate aminotransferase(AST) and total bilimbin(TBiL) were detected by automatic biochemistry analysator. The liver and bowel tissue was observed by lightmicroscope and transmission electron microscope(TEM). The apoptosis of hepatocyte was detected by TUNEL. HPLC-PED was used in the study of intestinal permeability. Result No significant differences were noted between ALT, AST, TBIL level, death rate and intestinal permeability(L/M) between model group and GLN pretreated group;In microscope, the confused structure of hepatic injury and inflammatory infiltration were similar between model group and GLN pretreated greup.The injury of bowel was not obviously. Compared with the model group, there was better trend in liver and bowel in GLN pretreated group by transmission electron microscope(TEM) .The apoptosis index in GLN pretreated group were lower than those in model group. Conclusion LPS can induce acute liver injury in D-Gal-sensitized rats. Glutamine has't the trend of protecting liver function and intestinal barrier function, decreasing death rates.