CAJ | 학술논문

背景:衰老大鼠静脉注射脂多糖后能导致肺损伤,进而发现随着肺损伤的进展,影响肾功能.银杏叶提取物具有一定的清除自由基、改善血液流变学和保护血管内皮细胞等功能. 目的:研究人工衰老大鼠肺损伤后是否发生肾功能不全,以验证老年多器官功能不全的肺启动机制,并观察银杏叶提取物对其是否有保护作用. 设计:以实验动物为观察对象的随机对照的实验. 单位:中国协和医科大学基础医学研究所病理生理学系. 材料:实验于2001-05/2003-01在中国协和医科大学基础医学研究所病理生理学系实验室完成.选用36只Wistar雄性大鼠. 方法:给大鼠每天1次经腹腔注入D-半乳糖(50 mg/kg),连续6周,复制衰老动物模型,再随机分为3组:对照组(静脉注射生理盐水);脂多糖组(静脉注射脂多糖,5 mg/kg);银杏叶提取物+脂多糖组(注射脂多糖前7 d开始,每天银杏叶提取物灌胃1次,31 mg/kg).各组大鼠在给生理盐水或脂多糖后2 h或6 h取血和肺、肾组织. 主要观察指标:用比色法测定血中肌酐、尿素氮含量;血、肺、肾组织中丙二醛、No2-/NO3-含量及谷胱甘肽过氧化物酶及Na+-K+-ATP酶活性的测定. 结果:衰老大鼠在注射脂多糖后2,6h时已形成急性肺损伤.注射脂多糖后2 h血中肌酐及尿素氮含量无明显升高,而6 h时均显著升高,分别为 (94.7±10.3)μmol/L,(11.4±1.9)mmol/L.在注射脂多糖后2h,血和肺组织中丙二醛[(22.5+2.6)nmol/L,(25.8±2.9)μmol/gl和No2-/NO3-含量[(58.5 ±6.8)mmol/L,(34.6±3.8μmol/g]均显著升高,而谷胱甘肽过氧化物酶 [(355.1±45.0)μkat/g]及Na+-K+-ATP酶[(886.3±97.1)nkat/g]下降.上述指标的变化持续至观察的6 h.而肾组织中上述指标仅在注射脂多糖后6 h才有显著性变化.银杏叶提取物可显著缓解上述指标的变化. 结论:脂多糖所致衰老大鼠的肺损伤可进一步诱导肾功能受损.银杏叶提取物对脂多糖诱发的衰老大鼠的急性肺损伤和由此诱导的肾功能受损有明显的保护作用. 揹景:衰老大鼠靜脈註射脂多糖後能導緻肺損傷,進而髮現隨著肺損傷的進展,影響腎功能.銀杏葉提取物具有一定的清除自由基、改善血液流變學和保護血管內皮細胞等功能. 目的:研究人工衰老大鼠肺損傷後是否髮生腎功能不全,以驗證老年多器官功能不全的肺啟動機製,併觀察銀杏葉提取物對其是否有保護作用. 設計:以實驗動物為觀察對象的隨機對照的實驗. 單位:中國協和醫科大學基礎醫學研究所病理生理學繫. 材料:實驗于2001-05/2003-01在中國協和醫科大學基礎醫學研究所病理生理學繫實驗室完成.選用36隻Wistar雄性大鼠. 方法:給大鼠每天1次經腹腔註入D-半乳糖(50 mg/kg),連續6週,複製衰老動物模型,再隨機分為3組:對照組(靜脈註射生理鹽水);脂多糖組(靜脈註射脂多糖,5 mg/kg);銀杏葉提取物+脂多糖組(註射脂多糖前7 d開始,每天銀杏葉提取物灌胃1次,31 mg/kg).各組大鼠在給生理鹽水或脂多糖後2 h或6 h取血和肺、腎組織. 主要觀察指標:用比色法測定血中肌酐、尿素氮含量;血、肺、腎組織中丙二醛、No2-/NO3-含量及穀胱甘肽過氧化物酶及Na+-K+-ATP酶活性的測定. 結果:衰老大鼠在註射脂多糖後2,6h時已形成急性肺損傷.註射脂多糖後2 h血中肌酐及尿素氮含量無明顯升高,而6 h時均顯著升高,分彆為 (94.7±10.3)μmol/L,(11.4±1.9)mmol/L.在註射脂多糖後2h,血和肺組織中丙二醛[(22.5+2.6)nmol/L,(25.8±2.9)μmol/gl和No2-/NO3-含量[(58.5 ±6.8)mmol/L,(34.6±3.8μmol/g]均顯著升高,而穀胱甘肽過氧化物酶 [(355.1±45.0)μkat/g]及Na+-K+-ATP酶[(886.3±97.1)nkat/g]下降.上述指標的變化持續至觀察的6 h.而腎組織中上述指標僅在註射脂多糖後6 h纔有顯著性變化.銀杏葉提取物可顯著緩解上述指標的變化. 結論:脂多糖所緻衰老大鼠的肺損傷可進一步誘導腎功能受損.銀杏葉提取物對脂多糖誘髮的衰老大鼠的急性肺損傷和由此誘導的腎功能受損有明顯的保護作用.
배경:쇠로대서정맥주사지다당후능도치폐손상,진이발현수착폐손상적진전,영향신공능.은행협제취물구유일정적청제자유기、개선혈액류변학화보호혈관내피세포등공능. 목적:연구인공쇠로대서폐손상후시부발생신공능불전,이험증노년다기관공능불전적폐계동궤제,병관찰은행협제취물대기시부유보호작용. 설계:이실험동물위관찰대상적수궤대조적실험. 단위:중국협화의과대학기출의학연구소병리생이학계. 재료:실험우2001-05/2003-01재중국협화의과대학기출의학연구소병리생이학계실험실완성.선용36지Wistar웅성대서. 방법:급대서매천1차경복강주입D-반유당(50 mg/kg),련속6주,복제쇠로동물모형,재수궤분위3조:대조조(정맥주사생리염수);지다당조(정맥주사지다당,5 mg/kg);은행협제취물+지다당조(주사지다당전7 d개시,매천은행협제취물관위1차,31 mg/kg).각조대서재급생리염수혹지다당후2 h혹6 h취혈화폐、신조직. 주요관찰지표:용비색법측정혈중기항、뇨소담함량;혈、폐、신조직중병이철、No2-/NO3-함량급곡광감태과양화물매급Na+-K+-ATP매활성적측정. 결과:쇠로대서재주사지다당후2,6h시이형성급성폐손상.주사지다당 후2 h혈중기항급뇨소담함량무명현승고,이6 h시균현저승고,분별위 (94.7±10.3)μmol/L,(11.4±1.9)mmol/L.재주사지다당후2h,혈화폐조직 중병이철[(22.5+2.6)nmol/L,(25.8±2.9)μmol/gl화No2-/NO3-함량[(58.5 ±6.8)mmol/L,(34.6±3.8μmol/g]균현저승고,이곡광감태과양화물매 [(355.1±45.0)μkat/g]급Na+-K+-ATP매[(886.3±97.1)nkat/g]하강.상술지표 적변화지속지관찰적6 h.이신조직중상술지표부재주사지다당후6 h재 유현저성변화.은행협제취물가현저완해상술지표적변화. 결론:지다당소치쇠로대서적폐손상가진일보유도신공능수손.은행협 제취물대지다당유발적쇠로대서적급성폐손상화유차유도적신공능수 손유명현적보호작용.
BACKGROUND:Lung injury can be induced after injection of lipopolysaccharide(LPS) into the vein of aging rats,and with the development of lung injury,the kidney function can be influenced.Ginkgo biloba extract(GBE) has some effects such as clearing the free radicals,improving hemorrheology,protecting the vascular endothelial cells and so on. OBJECTIVE:To investigate whether renal function damage is induced by acute lung injury(ALI) in aging rats so as to support the hypothesis that lung is the start-up organ in multiple organ dysfunction syndrome in the elderly and the protective effect of GBE on it. DESIGN:Randomized controlled experimental trial based on the experimental animals. SETTING:Laboratory of Department of Pathophysiology,Institute of Basic Medical Science,Peking Union Medical College. MATERIALS:The study has been completed from May 2001 to January 2003 in the Laboratory of Department of Pathophysiology,Institute of Basic Medical Science,Peking Union Medical College.Thirty-six Wistar male rats were involved. INTERVENTIONS:For reproducing the mimic aging rats models,the rats were injected intraperitoneally,D-gal 50 mg/kg,once a day,for 6weeks totally,and randomly divided into 3 groups, namely: ①control group(saline ,intravenous injection);② LPS group( LPS,5 mg/kg intravenous injection) ③ GBE+LPS group (GBE was used 7 days prior to LPS,31 mg/kg ,once a day).Samples(blood,lung and kidney tissue) were collected at 2 or 6 hours after LPS or saline administration. MAIN OUTCOME MEASURES:Contents of creatinine(Cr),blood urea nitrogen (BUN),lactic acid (LA),NO (its metabolite is NO2-/NO3-) and methane dicarboxylic aldehyde(MDA);and activities of glutathione peroxi-dase(GSH-Px) and Na+-K+-ATPase were measured. RESULTS:Compared with control group,there was obviously ALI at 2or 6 hours after LPS administration.Cr [(94.7±10.3) μmol/L]and BUN [(l1.4 1.9)mmol/L]contents in blood were increased significantly until 6 hours after LPS administration.In LPS group,MDA[(22.5 2.6) nmol/L]and NO2-/NO3-[(25.8 2.9) μmol/g] contents in blood and in lung tissue were all increased significantly at 2 hours.But GSH-PX [(355.1 45.0)μkat/g],Na+-K+-ATPase [(886.3 97.2) nkat/g] activities in lung tissue were decreased significantly at 2 hours after LPS administration.The above changes lasted for 6 hours.However,significant change did not occur until 6 hours after LPS administration in renal tissue.All the above changes were markedly attenuated by pretreatment of GBE. CONCLUSION:ALI was caused by LPS intravenous injection in aging rats.Renal function damage could be induced by ALI in aging rats.GBE showed a protective effect on ALI and renal function damage in this animal model.