中华航海医学与高气压医学杂志
中華航海醫學與高氣壓醫學雜誌
중화항해의학여고기압의학잡지
CHINESE JOURNAL OF NAUTICAL MEDICINE AND HYPERBARIC MEDICINE
2011年
5期
288-291
,共4页
周宏图%周红%严丽荣%袁建国%李绒%张雪春%周玉梅
週宏圖%週紅%嚴麗榮%袁建國%李絨%張雪春%週玉梅
주굉도%주홍%엄려영%원건국%리융%장설춘%주옥매
高压氧%老年痴呆%超氧化物歧化酶%丙二醛%谷胱甘肽%氧化应激
高壓氧%老年癡呆%超氧化物歧化酶%丙二醛%穀胱甘肽%氧化應激
고압양%노년치태%초양화물기화매%병이철%곡광감태%양화응격
Hyperbaric oxygen%Alzheimer disease%Superoxide dismutase (SOD)%Malondialdehyde (MDA)%Glutathione%Oxidative stress
目的 探讨高压氧对老年痴呆小鼠(AD)的抗痴呆作用.方法 将30只昆明种雄性小鼠按数字表法随机均分成3组:对照组(不作任何处理)、模型组(建成痴呆模型后不作任何处理)、高压氧组(建模后进行高压氧治疗),每组10只.后2组用D-半乳糖(120 mg/kg)和亚硝酸钠(90 mg/kg)联合制作老年痴呆小鼠模型,利用Morris水迷宫试验进行逃避潜伏期、跨越平台次数的检测;采用酶生化法和硫代巴比妥酸法进行血清超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活性和丙二醛(MDA)含量检测;取小鼠海马CA1区脑组织行HE染色,观察神经细胞形态变化.结果 与对照组比较,模型组逃避潜伏期[(76.13±25.28)s]明显延长(P<0.01),跨越平台次数[(2.34±0.87)次]明显减少(P<0.01),血清中SOD[ (269.70±33.45) U/ml]、GSH-Px[ (4.38±1.21) g/L]活性显著降低(P<0.01),MDA[ (6.57±2.04) μmol/L]含量显著升高(P<0.01),海马CA1区神经细胞排列稀疏、紊乱,出现大量退行性神经元;模型组经高压氧治疗后,与治疗前比较逃避潜伏期明显缩短(P<0.01)、跨越平台次数明显增多(P<0.01),血清SOD、GSH-Px活性显著升高(P<0.01),MDA含量显著降低(P<0.01),治疗前后差异均有统计学意义(P<0.01),而且海马CA1区正常神经细胞数量较治疗前明显增多、细胞排列紧密.结论 高压氧治疗可以显著提高痴呆模型鼠的抗自由基损伤能力,具有抗痴呆功能,对AD具有一定的治疗作用.
目的 探討高壓氧對老年癡呆小鼠(AD)的抗癡呆作用.方法 將30隻昆明種雄性小鼠按數字錶法隨機均分成3組:對照組(不作任何處理)、模型組(建成癡呆模型後不作任何處理)、高壓氧組(建模後進行高壓氧治療),每組10隻.後2組用D-半乳糖(120 mg/kg)和亞硝痠鈉(90 mg/kg)聯閤製作老年癡呆小鼠模型,利用Morris水迷宮試驗進行逃避潛伏期、跨越平檯次數的檢測;採用酶生化法和硫代巴比妥痠法進行血清超氧化物歧化酶(SOD)、穀胱甘肽過氧化物酶(GSH-Px)活性和丙二醛(MDA)含量檢測;取小鼠海馬CA1區腦組織行HE染色,觀察神經細胞形態變化.結果 與對照組比較,模型組逃避潛伏期[(76.13±25.28)s]明顯延長(P<0.01),跨越平檯次數[(2.34±0.87)次]明顯減少(P<0.01),血清中SOD[ (269.70±33.45) U/ml]、GSH-Px[ (4.38±1.21) g/L]活性顯著降低(P<0.01),MDA[ (6.57±2.04) μmol/L]含量顯著升高(P<0.01),海馬CA1區神經細胞排列稀疏、紊亂,齣現大量退行性神經元;模型組經高壓氧治療後,與治療前比較逃避潛伏期明顯縮短(P<0.01)、跨越平檯次數明顯增多(P<0.01),血清SOD、GSH-Px活性顯著升高(P<0.01),MDA含量顯著降低(P<0.01),治療前後差異均有統計學意義(P<0.01),而且海馬CA1區正常神經細胞數量較治療前明顯增多、細胞排列緊密.結論 高壓氧治療可以顯著提高癡呆模型鼠的抗自由基損傷能力,具有抗癡呆功能,對AD具有一定的治療作用.
목적 탐토고압양대노년치태소서(AD)적항치태작용.방법 장30지곤명충웅성소서안수자표법수궤균분성3조:대조조(불작임하처리)、모형조(건성치태모형후불작임하처리)、고압양조(건모후진행고압양치료),매조10지.후2조용D-반유당(120 mg/kg)화아초산납(90 mg/kg)연합제작노년치태소서모형,이용Morris수미궁시험진행도피잠복기、과월평태차수적검측;채용매생화법화류대파비타산법진행혈청초양화물기화매(SOD)、곡광감태과양화물매(GSH-Px)활성화병이철(MDA)함량검측;취소서해마CA1구뇌조직행HE염색,관찰신경세포형태변화.결과 여대조조비교,모형조도피잠복기[(76.13±25.28)s]명현연장(P<0.01),과월평태차수[(2.34±0.87)차]명현감소(P<0.01),혈청중SOD[ (269.70±33.45) U/ml]、GSH-Px[ (4.38±1.21) g/L]활성현저강저(P<0.01),MDA[ (6.57±2.04) μmol/L]함량현저승고(P<0.01),해마CA1구신경세포배렬희소、문란,출현대량퇴행성신경원;모형조경고압양치료후,여치료전비교도피잠복기명현축단(P<0.01)、과월평태차수명현증다(P<0.01),혈청SOD、GSH-Px활성현저승고(P<0.01),MDA함량현저강저(P<0.01),치료전후차이균유통계학의의(P<0.01),이차해마CA1구정상신경세포수량교치료전명현증다、세포배렬긴밀.결론 고압양치료가이현저제고치태모형서적항자유기손상능력,구유항치태공능,대AD구유일정적치료작용.
Objective To study the effect of hyperbaric oxygen on the anti-senility of mice with Alzheimer disease.Methods Thirty male KM mice were randomly divided into 3 groups:the control group,the model group and the HBO group.Models of dementia mice were successfully developed with D-galactose (120 mg/kg) and sodium nitrite (90 mg/kg).Escape latency and times of running across the platform were respectively determined by Morris water maze.The activity of serum superoxide dismutase (SOD),glutathione peroxide (GSH-Px) and the content of malondialdehyde (MDA) were detected with biochemical enzyme and thiobarbituric acid.Morphology of neurons in the hippocampal CA1 region was observed with H&E staining.Results When compared with that of the control group,the escape latency for the model group obviously prolonged [ (76.13 ± 25.28 ) s ] (P < 0.01 ),times of running across the platform reduced [ ( 2.34 ± 0.87 )times ] (P < 0.01 ),the activity of SOD [ ( 269.70 ± 33.45 ) U/ml ] and GSH-Px [ (4.38 ± 1.21 ) g/L ]significantly decreased,but the content of MDA increased [ (6.57 ±2.04) μmol/L] (P <0.01 ).A great amount of degenerative neurons and sparse irregular cell arrangements could be detected in hippocampal CA1region in the dementia mice.Following HBO treatment,the escape latency shortened,the times of running across the platform increased,the activity of SOD and GSH-Px significantly increased,while the content of MDA decreased,with statistical significance (P <0.01 ).The No.of normal cells in the hippocampal CA1 region increased significantly,when compared with that of HBO treatment,and the neurons in the CA1 region were tightly arranged.Conclusions HBO could obviously increase the capacity of the mice with AD to alleviate lesion induced by oxygen free radicals and has certain effect on the treatment of AD through anti-senile mechanism.