重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2014年
23期
3037-3039
,共3页
谢丽萍%代志刚%王胜%刘扬%董希玮%张振英
謝麗萍%代誌剛%王勝%劉颺%董希瑋%張振英
사려평%대지강%왕성%류양%동희위%장진영
p38丝裂原活化蛋白激酶%舒芬太尼%肝脏%缺血再灌注损伤%应激反应
p38絲裂原活化蛋白激酶%舒芬太尼%肝髒%缺血再灌註損傷%應激反應
p38사렬원활화단백격매%서분태니%간장%결혈재관주손상%응격반응
p38 mitogen activated protein kinase%sufentanil%hepatic%ischemia-reperfusion injury%stress response
目的:研究舒芬太尼预处理对大鼠肝脏缺血再灌注损伤的保护作用及其可能的作用机制。方法健康SD大鼠30只,雌雄不拘,体质量220~270g,随机分为5组(n=6):假手术组(Ⅰ组);肝缺血再灌注组(Ⅱ组);5μg/kg舒芬太尼预处理组(Ⅲ组);p38丝裂原活化蛋白激酶(p38MAPK)阻断剂SB203580+Ⅲ组(Ⅳ组)和溶解剂二甲基亚砜(DMSO)组(Ⅴ组),至灌注240min时取材。抽取腹主动脉血测定血清中谷丙转氨酶(ALT)和谷草转氨酶(AST)活性;处死大鼠,收集肝组织,观察肝组织丙二醛(MDA)和超氧化物歧化酶(SOD)的变化;光学显微镜下观察肝组织病理学改变;Westernblotting法测定肝右叶组织p-p38MAPK的表达水平。结果与Ⅰ组相比,Ⅱ~Ⅴ组血清ALT、AST,肝组织MDA水平显著升高,出现病理学损伤;与Ⅱ组相比,Ⅲ组血清ALT、AST及肝组织MDA水平均明显下降,肝组织SOD水平明显升高,病理学损伤减轻,p-p38MAPK表达明显升高;与Ⅲ组相比,应用p38MAPK阻断剂SB203580,肝损伤加重;Ⅴ组与Ⅱ组各指标比较差异无统计学意义(P>0.05)。结论舒芬太尼预处理可减轻大鼠肝缺血再灌注损伤,其机制可能是通过激活p38MAPK信号通路发挥作用。
目的:研究舒芬太尼預處理對大鼠肝髒缺血再灌註損傷的保護作用及其可能的作用機製。方法健康SD大鼠30隻,雌雄不拘,體質量220~270g,隨機分為5組(n=6):假手術組(Ⅰ組);肝缺血再灌註組(Ⅱ組);5μg/kg舒芬太尼預處理組(Ⅲ組);p38絲裂原活化蛋白激酶(p38MAPK)阻斷劑SB203580+Ⅲ組(Ⅳ組)和溶解劑二甲基亞砜(DMSO)組(Ⅴ組),至灌註240min時取材。抽取腹主動脈血測定血清中穀丙轉氨酶(ALT)和穀草轉氨酶(AST)活性;處死大鼠,收集肝組織,觀察肝組織丙二醛(MDA)和超氧化物歧化酶(SOD)的變化;光學顯微鏡下觀察肝組織病理學改變;Westernblotting法測定肝右葉組織p-p38MAPK的錶達水平。結果與Ⅰ組相比,Ⅱ~Ⅴ組血清ALT、AST,肝組織MDA水平顯著升高,齣現病理學損傷;與Ⅱ組相比,Ⅲ組血清ALT、AST及肝組織MDA水平均明顯下降,肝組織SOD水平明顯升高,病理學損傷減輕,p-p38MAPK錶達明顯升高;與Ⅲ組相比,應用p38MAPK阻斷劑SB203580,肝損傷加重;Ⅴ組與Ⅱ組各指標比較差異無統計學意義(P>0.05)。結論舒芬太尼預處理可減輕大鼠肝缺血再灌註損傷,其機製可能是通過激活p38MAPK信號通路髮揮作用。
목적:연구서분태니예처리대대서간장결혈재관주손상적보호작용급기가능적작용궤제。방법건강SD대서30지,자웅불구,체질량220~270g,수궤분위5조(n=6):가수술조(Ⅰ조);간결혈재관주조(Ⅱ조);5μg/kg서분태니예처리조(Ⅲ조);p38사렬원활화단백격매(p38MAPK)조단제SB203580+Ⅲ조(Ⅳ조)화용해제이갑기아풍(DMSO)조(Ⅴ조),지관주240min시취재。추취복주동맥혈측정혈청중곡병전안매(ALT)화곡초전안매(AST)활성;처사대서,수집간조직,관찰간조직병이철(MDA)화초양화물기화매(SOD)적변화;광학현미경하관찰간조직병이학개변;Westernblotting법측정간우협조직p-p38MAPK적표체수평。결과여Ⅰ조상비,Ⅱ~Ⅴ조혈청ALT、AST,간조직MDA수평현저승고,출현병이학손상;여Ⅱ조상비,Ⅲ조혈청ALT、AST급간조직MDA수평균명현하강,간조직SOD수평명현승고,병이학손상감경,p-p38MAPK표체명현승고;여Ⅲ조상비,응용p38MAPK조단제SB203580,간손상가중;Ⅴ조여Ⅱ조각지표비교차이무통계학의의(P>0.05)。결론서분태니예처리가감경대서간결혈재관주손상,기궤제가능시통과격활p38MAPK신호통로발휘작용。
Objective To study the protective effect of sufentanil preconditioning on hepatic ischemia-reperfusion injury in rats and to investigate the mechanisms whether may be by activating p38 MAPK signal pathway to promote p38 MAPK phosphoryla-tion .Methods Thirty SD rats(in either gender ,weighing 220-270 g) were randomly divided into five groups :Sham-operated group (Ⅰ) ,ischemia-reperfusion group(Ⅱ);sufentanil preconditioning group(5 μg/kg ,Ⅲ) ,SB203580(an inhibitor of p38 MAPK) group (Ⅳ) ,and dimethyl sulphoxide (DMSO) control group(Ⅴ) .Sample specimens were collected from each group at 240 minutes after reperfusion .Serum alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were measured by an automatic biochem-ical analyzer .Malondialdehyde(MDA) and superoxide dismutase(SOD) in liver tissue was measured .HE staining was used to ob-serve the hepatic pathological changes ,and to examine the expression of phosphor-p38 mitogen-activated protein kinases (p-p38 MAPK)of hepatic tissues by western blotting .Results Compared with group Ⅰ ,levels of AST ,ALT and MDA showed signifi-cantly increased in group Ⅱ-Ⅴ ,but levels of SOD decreased ,and obvious pathological changes were observed in the liver .In GroupⅢ significantly decreased the elevated levels of ASL ,ALT and MDA but increased levels of SOD ,and lessened hepatic pathological changes ,caused promoted p38 MAPK phosphorylation at 240 minutes after reperfusion .The protective effects of sufentanil precon-ditioning were abolished by SB203580 pretreatment .There were no significant differences between group Ⅴ and group Ⅱ .Conclu-sion Sufentanil preconditioning can reduce the hepatic ischemia-reperfusion injury .The protective mechanisms may be by activating p38 MAPK signal pathway to promote p38 MAPK phosphorylation .