中国老年学杂志
中國老年學雜誌
중국노년학잡지
CHINESE JOURNAL OF GERONTOLOGY
2009年
23期
3064-3066
,共3页
李鹏%易斌%王秀琼%罗铁山%石胜驰%许广明%陶国才
李鵬%易斌%王秀瓊%囉鐵山%石勝馳%許廣明%陶國纔
리붕%역빈%왕수경%라철산%석성치%허엄명%도국재
异氟醚%氧化性应激%高级糖基化终产物%丙二醛%超氧化物歧化酶
異氟醚%氧化性應激%高級糖基化終產物%丙二醛%超氧化物歧化酶
이불미%양화성응격%고급당기화종산물%병이철%초양화물기화매
Isoflurane%Oxidative stress%Advanced glycosylation end products%Malondialdehyde%Superoxide dismutase
目的 研究异氟醚对老年大鼠脑组织高级糖基化终末产物(AGEs)及氧化应激水平的影响.方法 老年及成年SD雄性大鼠共32只,在安静无干扰环境中进行12 h/12 h光暗周期节律适应4 d后,随机分为老年对照组(N1组),老年异氟醚处理组(A1组),成年对照组(N2组),成年异氟醚处理组(A2组).异氟醚组均给予异氟醚吸入处理3 h,对照组在相同时间,安静环境呼吸空气3 h.免疫组织化学法测定大鼠海马AGEs水平变化,硫代巴比妥法(TBA)测定脑组织丙二醛(MDA)含量,黄嘌呤氧化酶法测定超氧化物歧化酶(SOD)活性.结果 与N2组比较,N1组大鼠脑内AGEs、 MDA基础水平较高,SOD活性低于N2组. 24 h后A1组海马AGEs水平较N1组及A2组明显升高(P<0.01);A2组AGEs水平与N2组比较无显著变化(P>0.05).A1组MDA含量为(10.35±0.62)nmol/mg,较N1组及A2组明显升高,而SOD活性降低(P<0.01).A2组SOD活性为(104.45±11.26) U/mg,较N2组降低,而MDA活性较A2组升高(P<0.05).结论 异氟醚处理可引起老年大鼠脑组织内AGEs增高及氧化应激水平进一步升高可能是老年术后认知功能紊乱的机制之一.
目的 研究異氟醚對老年大鼠腦組織高級糖基化終末產物(AGEs)及氧化應激水平的影響.方法 老年及成年SD雄性大鼠共32隻,在安靜無榦擾環境中進行12 h/12 h光暗週期節律適應4 d後,隨機分為老年對照組(N1組),老年異氟醚處理組(A1組),成年對照組(N2組),成年異氟醚處理組(A2組).異氟醚組均給予異氟醚吸入處理3 h,對照組在相同時間,安靜環境呼吸空氣3 h.免疫組織化學法測定大鼠海馬AGEs水平變化,硫代巴比妥法(TBA)測定腦組織丙二醛(MDA)含量,黃嘌呤氧化酶法測定超氧化物歧化酶(SOD)活性.結果 與N2組比較,N1組大鼠腦內AGEs、 MDA基礎水平較高,SOD活性低于N2組. 24 h後A1組海馬AGEs水平較N1組及A2組明顯升高(P<0.01);A2組AGEs水平與N2組比較無顯著變化(P>0.05).A1組MDA含量為(10.35±0.62)nmol/mg,較N1組及A2組明顯升高,而SOD活性降低(P<0.01).A2組SOD活性為(104.45±11.26) U/mg,較N2組降低,而MDA活性較A2組升高(P<0.05).結論 異氟醚處理可引起老年大鼠腦組織內AGEs增高及氧化應激水平進一步升高可能是老年術後認知功能紊亂的機製之一.
목적 연구이불미대노년대서뇌조직고급당기화종말산물(AGEs)급양화응격수평적영향.방법 노년급성년SD웅성대서공32지,재안정무간우배경중진행12 h/12 h광암주기절률괄응4 d후,수궤분위노년대조조(N1조),노년이불미처리조(A1조),성년대조조(N2조),성년이불미처리조(A2조).이불미조균급여이불미흡입처리3 h,대조조재상동시간,안정배경호흡공기3 h.면역조직화학법측정대서해마AGEs수평변화,류대파비타법(TBA)측정뇌조직병이철(MDA)함량,황표령양화매법측정초양화물기화매(SOD)활성.결과 여N2조비교,N1조대서뇌내AGEs、 MDA기출수평교고,SOD활성저우N2조. 24 h후A1조해마AGEs수평교N1조급A2조명현승고(P<0.01);A2조AGEs수평여N2조비교무현저변화(P>0.05).A1조MDA함량위(10.35±0.62)nmol/mg,교N1조급A2조명현승고,이SOD활성강저(P<0.01).A2조SOD활성위(104.45±11.26) U/mg,교N2조강저,이MDA활성교A2조승고(P<0.05).결론 이불미처리가인기노년대서뇌조직내AGEs증고급양화응격수평진일보승고가능시노년술후인지공능문란적궤제지일.
Objective To investigate the effects of isoflurane on advanced glycation end products (AGEs) and oxidative stress levels in the rat brain. Methods 32 male SD rats were randomly divided into 4 groups: old age control group(N1), old isoflurane anesthesia group(A1), adult control group(N2), adult isoflurane anesthesia group(A2). Anesthesia groups were given inhaled isoflurane anesthesia for 3 hours meanwhile breathing the air in the control group. The animals were killed 24 hours after anesthesia to detect the AGEs in the hippocampus tissues by immunohistochemistry. Brain tissue malondialdehyde(MDA)and superoxide dismutase(SOD)were detected by colorimetric. Results Compared with N2 group, the basis of the levels of AGEs and MDA were higher but SOD activity was lower in N1 group. Compared with N1 and A2 group, the hippocampal levels of AGEs were significantly higher in group A1 after 24 hours (P<0.01). There was no significant difference in AGEs levels between N2 and A2 group (P>0.05). Compared with N1 and A2 group, MDA increased significantly and SOD activity decreased in A1 group (P<0.01).Compared with N2 group, MDA were higher and SOD activity were lower in A2 group(P<0.05). Conclusions Isoflurane can increase the expression of AGEs and the levels of oxidative stress in hippocampus of aged rats. The changes may be one of the mechanisms of old postoperative cognitive dysfunction patients.