中国医药导报
中國醫藥導報
중국의약도보
CHINA MEDICAL HERALD
2014年
24期
36-40
,共5页
任歆%黄蕊%成学恭%李光来
任歆%黃蕊%成學恭%李光來
임흠%황예%성학공%리광래
血糖%脑缺血-再灌注%氧化应激
血糖%腦缺血-再灌註%氧化應激
혈당%뇌결혈-재관주%양화응격
Blood glucose%Ischemia-reperfusion%Oxidative stress
目的：探讨在缺血再灌注脑损伤动物模型中血糖水平对氧化应激反应的影响。方法采用结扎大鼠两侧颈总动脉的急性脑缺血再灌注模型，Wistar雄性大鼠随机分为4组：假手术组(A组)、生理盐水对照组(B组)、胰岛素组(2.1 U/kg，C组)、胰岛素(2.1 U/kg)+50%葡萄糖(2 g/kg)组(D组)。术后取标本切片观察脑组织超微结构的变化，并检测脑组织中丙二醛(MDA，脂质过氧化产物)、超氧化物歧化酶(SOD)含量及ATP酶活性。结果①A、D组血糖正常(4.6~10 mmol/L)，与之相比，B组血糖升高明显(P<0.01)，C组血糖下降明显(P<0.01)；②脑组织内MDA、SOD含量及ATP酶活性，B组与C组相比差异无统计学意义(P>0.05)，同B组相比，D组血糖水平在正常值的高限可以降低脑组织中MDA含量(P<0.05)，升高SOD水平(P<0.05)，提高ATP酶活性(P<0.05)。结论①脑缺血再灌注损伤可以导致血糖水平升高并产生氧化应激损伤；②缺血再灌注时低血糖也可以加剧氧化应激反应；③缺血再灌注后控制血糖至正常值的高限可以减轻氧化应激反应。
目的：探討在缺血再灌註腦損傷動物模型中血糖水平對氧化應激反應的影響。方法採用結扎大鼠兩側頸總動脈的急性腦缺血再灌註模型，Wistar雄性大鼠隨機分為4組：假手術組(A組)、生理鹽水對照組(B組)、胰島素組(2.1 U/kg，C組)、胰島素(2.1 U/kg)+50%葡萄糖(2 g/kg)組(D組)。術後取標本切片觀察腦組織超微結構的變化，併檢測腦組織中丙二醛(MDA，脂質過氧化產物)、超氧化物歧化酶(SOD)含量及ATP酶活性。結果①A、D組血糖正常(4.6~10 mmol/L)，與之相比，B組血糖升高明顯(P<0.01)，C組血糖下降明顯(P<0.01)；②腦組織內MDA、SOD含量及ATP酶活性，B組與C組相比差異無統計學意義(P>0.05)，同B組相比，D組血糖水平在正常值的高限可以降低腦組織中MDA含量(P<0.05)，升高SOD水平(P<0.05)，提高ATP酶活性(P<0.05)。結論①腦缺血再灌註損傷可以導緻血糖水平升高併產生氧化應激損傷；②缺血再灌註時低血糖也可以加劇氧化應激反應；③缺血再灌註後控製血糖至正常值的高限可以減輕氧化應激反應。
목적：탐토재결혈재관주뇌손상동물모형중혈당수평대양화응격반응적영향。방법채용결찰대서량측경총동맥적급성뇌결혈재관주모형，Wistar웅성대서수궤분위4조：가수술조(A조)、생리염수대조조(B조)、이도소조(2.1 U/kg，C조)、이도소(2.1 U/kg)+50%포도당(2 g/kg)조(D조)。술후취표본절편관찰뇌조직초미결구적변화，병검측뇌조직중병이철(MDA，지질과양화산물)、초양화물기화매(SOD)함량급ATP매활성。결과①A、D조혈당정상(4.6~10 mmol/L)，여지상비，B조혈당승고명현(P<0.01)，C조혈당하강명현(P<0.01)；②뇌조직내MDA、SOD함량급ATP매활성，B조여C조상비차이무통계학의의(P>0.05)，동B조상비，D조혈당수평재정상치적고한가이강저뇌조직중MDA함량(P<0.05)，승고SOD수평(P<0.05)，제고ATP매활성(P<0.05)。결론①뇌결혈재관주손상가이도치혈당수평승고병산생양화응격손상；②결혈재관주시저혈당야가이가극양화응격반응；③결혈재관주후공제혈당지정상치적고한가이감경양화응격반응。
Objective To discuss the influence of blood glucose on oxidative stress in animal cerebral ischemic-reper-fusion models. Methods Acute cerebral ischemia-reperfusion models were made by bilateral carotid artery ligation for 30 minutes and then reperfusion for 2 hours. Male Wistar rats were randomly divided into 4 groups: sham operation group (group A), normal saline control group (group B), insulin group (2.1 U/kg, group C), insulin (2.1 U/kg) and 50%glucose (2 g/kg) group (group D). After operation, the brain tissue specimens were sectioned to observe the change of ultrastructure. The content of methane dicarboxylic aldehyde (MDA, product of lipid peroxidation), superoxide dismu-tase (SOD), and the activity of ATP enzyme were detected. Results ①Blood glucose levels in group A and D were within normal limits (4.6-10 mmol/L), blood glucose in group B increased significantly (P< 0.01), blood glucose in group C decreased significantly (P<0.01);②MDA and SOD content, ATP-ase activity in brain tissue of group B and group C had no significant difference (P>0.05);compared with the group B, MDA was reduced (P<0.05), SOD was elevated (P< 0.05), and ATP-ase activity was increased (P< 0.05) in group D. Conclusion ①Cerebral ischemia-reperfusion can increase blood glucose, and cause oxidative stress in cerebral tissue. ②During ischemia reperfusion, if blood glucose level is too low, can aggravate oxidative stress. ③Control blood glucose to upper limit of normal range can reduce oxidative stress.
