中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
Chinese Journal of Emergency Medicine
2015年
9期
964-968
,共5页
樊斌%石乔%刘黎明%王卫星
樊斌%石喬%劉黎明%王衛星
번빈%석교%류려명%왕위성
氢饱和生理盐水%胰腺炎%肺损伤%保护作用%P38MAPK%NF-κB
氫飽和生理鹽水%胰腺炎%肺損傷%保護作用%P38MAPK%NF-κB
경포화생리염수%이선염%폐손상%보호작용%P38MAPK%NF-κB
Hydrogen-rich saline%Pancreatitis%Lung injury%Protective effect%P38MAPK%NF-κB
目的 探讨氢饱和生理盐水对重症急性胰腺炎大鼠肺损伤的保护作用及其对P38MAPK和NF-κB表达的影响.方法 雄性Wistar大鼠54只,随机数字法分为假手术组(SO组)、重症急性胰腺炎组(SAP组)和氢饱和生理盐水处理组(HRS组),每组大鼠18只.胆胰管逆行注射5％牛磺胆酸钠制备重症急性胰腺炎模型.HRS组在造模成功后5 min尾静脉注射HRS(6 mL/kg),并皮下HRS补液(20 mL/kg).SO组、SAP组则在模型成功后5 min经尾静脉注射生理盐水(6 mL/kg),并皮下生理盐水补液(20 mL/kg).术后3、12、24 h分批剖杀大鼠,每个时间点6只.分别检测各组大鼠血清淀粉酶(AMY)、脂肪酶(LIP)水平.取新鲜肺组织检测其湿/干比(W/D).取肺组织病理切片行光镜观察及病理评分.采用免疫组化法检测P38MAPK、p-P38MAPK及NF-κB的表达.结果 HRS组各时间点血清AMY [12 h(5306.7 ±909)vs.(5 435.0 ±441.2)]、LIP [12 h(1 897.8±149.4)vs.(1917.9±106.8)]水平较SAP组相应时间点,差异无统计学意义(P＞0.05),肺组织W/D [12h (3.12±0.58)vs.(1.87±0.25)]及病理评分[12h (2.14±0.38)vs(3.58±0.32)]较SAP组相应时间点显著降低(P＜0.05).肺组织12 h时间点P38MAPK的表达在各组间差异无统计学意义;SAP组p-P38MAPK及NF-κB的表达较SO组显著升高,HRS组p-P38MAPK及NF-κB的表达较SAP组显著降低.结论 氢饱和生理盐水对重症急性胰腺炎肺损伤具有保护作用,其机制可能与抗氧化作用以及抑制P38MAPK、NF-κB激活有关.
目的 探討氫飽和生理鹽水對重癥急性胰腺炎大鼠肺損傷的保護作用及其對P38MAPK和NF-κB錶達的影響.方法 雄性Wistar大鼠54隻,隨機數字法分為假手術組(SO組)、重癥急性胰腺炎組(SAP組)和氫飽和生理鹽水處理組(HRS組),每組大鼠18隻.膽胰管逆行註射5％牛磺膽痠鈉製備重癥急性胰腺炎模型.HRS組在造模成功後5 min尾靜脈註射HRS(6 mL/kg),併皮下HRS補液(20 mL/kg).SO組、SAP組則在模型成功後5 min經尾靜脈註射生理鹽水(6 mL/kg),併皮下生理鹽水補液(20 mL/kg).術後3、12、24 h分批剖殺大鼠,每箇時間點6隻.分彆檢測各組大鼠血清澱粉酶(AMY)、脂肪酶(LIP)水平.取新鮮肺組織檢測其濕/榦比(W/D).取肺組織病理切片行光鏡觀察及病理評分.採用免疫組化法檢測P38MAPK、p-P38MAPK及NF-κB的錶達.結果 HRS組各時間點血清AMY [12 h(5306.7 ±909)vs.(5 435.0 ±441.2)]、LIP [12 h(1 897.8±149.4)vs.(1917.9±106.8)]水平較SAP組相應時間點,差異無統計學意義(P＞0.05),肺組織W/D [12h (3.12±0.58)vs.(1.87±0.25)]及病理評分[12h (2.14±0.38)vs(3.58±0.32)]較SAP組相應時間點顯著降低(P＜0.05).肺組織12 h時間點P38MAPK的錶達在各組間差異無統計學意義;SAP組p-P38MAPK及NF-κB的錶達較SO組顯著升高,HRS組p-P38MAPK及NF-κB的錶達較SAP組顯著降低.結論 氫飽和生理鹽水對重癥急性胰腺炎肺損傷具有保護作用,其機製可能與抗氧化作用以及抑製P38MAPK、NF-κB激活有關.
목적 탐토경포화생리염수대중증급성이선염대서폐손상적보호작용급기대P38MAPK화NF-κB표체적영향.방법 웅성Wistar대서54지,수궤수자법분위가수술조(SO조)、중증급성이선염조(SAP조)화경포화생리염수처리조(HRS조),매조대서18지.담이관역행주사5％우광담산납제비중증급성이선염모형.HRS조재조모성공후5 min미정맥주사HRS(6 mL/kg),병피하HRS보액(20 mL/kg).SO조、SAP조칙재모형성공후5 min경미정맥주사생리염수(6 mL/kg),병피하생리염수보액(20 mL/kg).술후3、12、24 h분비부살대서,매개시간점6지.분별검측각조대서혈청정분매(AMY)、지방매(LIP)수평.취신선폐조직검측기습/간비(W/D).취폐조직병리절편행광경관찰급병리평분.채용면역조화법검측P38MAPK、p-P38MAPK급NF-κB적표체.결과 HRS조각시간점혈청AMY [12 h(5306.7 ±909)vs.(5 435.0 ±441.2)]、LIP [12 h(1 897.8±149.4)vs.(1917.9±106.8)]수평교SAP조상응시간점,차이무통계학의의(P＞0.05),폐조직W/D [12h (3.12±0.58)vs.(1.87±0.25)]급병리평분[12h (2.14±0.38)vs(3.58±0.32)]교SAP조상응시간점현저강저(P＜0.05).폐조직12 h시간점P38MAPK적표체재각조간차이무통계학의의;SAP조p-P38MAPK급NF-κB적표체교SO조현저승고,HRS조p-P38MAPK급NF-κB적표체교SAP조현저강저.결론 경포화생리염수대중증급성이선염폐손상구유보호작용,기궤제가능여항양화작용이급억제P38MAPK、NF-κB격활유관.
Objective To investigate the protective effect of hydrogen-rich saline on lung injury associated with severe acute pancreatitis and its impact on P38MAPK and NF-κB expressions.Methods Fifty-four male Wistar rats were randomly (random number) divided into three groups:(1) hydrogen-rich saline treatment group (HRS group,n =18),in which the rats were treated with hydrogen-rich saline (6 mL/kg) administered intravenously via tail vein and HRS (20 mL/kg) administered subcutaneously at 5 min after successful modeling.(2) Severe acute pancreatitis model group (SAP group,n =18),in which rats received equivalent volume of normal saline instead of hydrogen-rich saline both intravenously and subcutaneously as in HRS group.(3) Sham operation group (SO group,n =18),in which rats were treated with sham surgery,and received equivalent volume of normal saline as in SAP group.The model of severe acute pancreatitis (SAP) was made by retrograde injection of 5％ sodium taurocholate (1 mL/kg) into cholepancreatic duct.All rats were sacrificed at 3 h,12 h,and 24 h separately after the operation (n =6 at a time).The levels of serum amylase,lipase were measured.The ratio of wet and dry lung tissues was measured.The histopathological changes of lung tissues were observed under optic microscope.The expressions of P38MAPK,p-P38MAPK and NF-κB were measured by using immunohistochemistry method.Results Compared with SAP group,there were no significant differences in levels of serum amylase [12 h (5306.7±909) vs.(5435.0 ±441.2)] and lipase [12 h (1897.8 ±149.4) vs.(1917.9± 106.8)] in HRS group (P ＞0.05),but there were significant differences in the ratio of wet and dry lung tissues [12 h (3.12 ± 0.58) vs.(1.87 ± 0.25)] and histopathology scores [12 h (2.14 ± 0.38) vs.(3.58 ±0.32)] (P ＜0.05).There was no significant difference in expression of P38MAPK in lung tissues among three groups at 12 h.Compared with SO group,the expressions of p-P38MAPK and NF-κB were significant increased in SAP group at 12 h,however,they were lower significantly in HRS group than those in SAP group.Conclusions Hydrogen-rich saline has a protective effect on lung injury associated with severe acute pancreatitis,and its mechanism may be likely related to the antioxidant effect and inhibiting the activation of P38MAPK and NF-κB.
