中国危重病急救医学
中國危重病急救醫學
중국위중병급구의학
CHINESE CRITICAL CARE MEDICINE
2010年
10期
587-590,前插7
,共5页
何美霞%曾进胜%华海婴%刑世会%巴云鹏
何美霞%曾進勝%華海嬰%刑世會%巴雲鵬
하미하%증진성%화해영%형세회%파운붕
脑梗死%丘脑腹后外侧核%DNA修复酶%抗氧化剂%大鼠
腦梗死%丘腦腹後外側覈%DNA脩複酶%抗氧化劑%大鼠
뇌경사%구뇌복후외측핵%DNA수복매%항양화제%대서
Cerebral infarction%Ventroposterior nucleus of the thalamus%DNA repair enzyme%Antioxidant%Rat
目的 观察大鼠大脑皮质梗死后丘脑腹后外侧核(VPN)继发性损害机制,以及抗氧化剂依布硒啉对脑损伤的改善作用.方法 采用易卒中型肾血管性高血压大鼠(RHRSP)建立大脑中动脉闭塞(MCAO)模型.按随机数字表法将大鼠分为假手术组、模型组、溶剂组、依布硒啉组,每组8只.假手术组仅暴露大脑中动脉不结扎;溶剂组和依布硒啉组术后24 h分别灌胃0.5%羧甲基纤维素钠+0.02%吐温20的溶剂或依布硒啉各5 ml/kg.2周后处死大鼠取脑组织,用苏木素-伊红(HE)染色观察VPN细胞形态;用免疫组化法观察无嘌呤无嘧啶核酸内切酶(APE)和大肠杆菌MutY DNA转葡萄糖基酶(MYH)两种DNA修复酶的表达.结果 HE染色显示依布硒啉可以改善皮质梗死所致的VPN细胞形态异常;免疫组化显示APE定位于VPN的胞核,MYH定位于VPN的胞质和胞核.模型组和溶剂组VPN的APE和MYH阳性细胞数(个)较假手术组显著减少(APE:57.0±14.7、49.4±12.5比101.0±13.6,MYH:15.0±4.7、10.4±2.5比56.0±13.2,均P＜0.05);依布硒啉组APE和MYH阳性细胞数较模型组和溶剂组显著增多(APE:72.2±7.6比57.0±14.7、49.4±12.5,MYH:32.2±7.6比15.0±4.7、10.4±2.5,均P＜0.05);模型组与溶剂组间APE和MYH阳性细胞数比较差异均无统计学意义.结论 实验性大鼠大脑皮质梗死后2周,VPN的DNA修复酶APE和MYH水平明显下降,抗氧化剂依布硒啉可明显升高其水平,从而阻止受损细胞死亡.
目的 觀察大鼠大腦皮質梗死後丘腦腹後外側覈(VPN)繼髮性損害機製,以及抗氧化劑依佈硒啉對腦損傷的改善作用.方法 採用易卒中型腎血管性高血壓大鼠(RHRSP)建立大腦中動脈閉塞(MCAO)模型.按隨機數字錶法將大鼠分為假手術組、模型組、溶劑組、依佈硒啉組,每組8隻.假手術組僅暴露大腦中動脈不結扎;溶劑組和依佈硒啉組術後24 h分彆灌胃0.5%羧甲基纖維素鈉+0.02%吐溫20的溶劑或依佈硒啉各5 ml/kg.2週後處死大鼠取腦組織,用囌木素-伊紅(HE)染色觀察VPN細胞形態;用免疫組化法觀察無嘌呤無嘧啶覈痠內切酶(APE)和大腸桿菌MutY DNA轉葡萄糖基酶(MYH)兩種DNA脩複酶的錶達.結果 HE染色顯示依佈硒啉可以改善皮質梗死所緻的VPN細胞形態異常;免疫組化顯示APE定位于VPN的胞覈,MYH定位于VPN的胞質和胞覈.模型組和溶劑組VPN的APE和MYH暘性細胞數(箇)較假手術組顯著減少(APE:57.0±14.7、49.4±12.5比101.0±13.6,MYH:15.0±4.7、10.4±2.5比56.0±13.2,均P＜0.05);依佈硒啉組APE和MYH暘性細胞數較模型組和溶劑組顯著增多(APE:72.2±7.6比57.0±14.7、49.4±12.5,MYH:32.2±7.6比15.0±4.7、10.4±2.5,均P＜0.05);模型組與溶劑組間APE和MYH暘性細胞數比較差異均無統計學意義.結論 實驗性大鼠大腦皮質梗死後2週,VPN的DNA脩複酶APE和MYH水平明顯下降,抗氧化劑依佈硒啉可明顯升高其水平,從而阻止受損細胞死亡.
목적 관찰대서대뇌피질경사후구뇌복후외측핵(VPN)계발성손해궤제,이급항양화제의포서람대뇌손상적개선작용.방법 채용역졸중형신혈관성고혈압대서(RHRSP)건립대뇌중동맥폐새(MCAO)모형.안수궤수자표법장대서분위가수술조、모형조、용제조、의포서람조,매조8지.가수술조부폭로대뇌중동맥불결찰;용제조화의포서람조술후24 h분별관위0.5%최갑기섬유소납+0.02%토온20적용제혹의포서람각5 ml/kg.2주후처사대서취뇌조직,용소목소-이홍(HE)염색관찰VPN세포형태;용면역조화법관찰무표령무밀정핵산내절매(APE)화대장간균MutY DNA전포도당기매(MYH)량충DNA수복매적표체.결과 HE염색현시의포서람가이개선피질경사소치적VPN세포형태이상;면역조화현시APE정위우VPN적포핵,MYH정위우VPN적포질화포핵.모형조화용제조VPN적APE화MYH양성세포수(개)교가수술조현저감소(APE:57.0±14.7、49.4±12.5비101.0±13.6,MYH:15.0±4.7、10.4±2.5비56.0±13.2,균P＜0.05);의포서람조APE화MYH양성세포수교모형조화용제조현저증다(APE:72.2±7.6비57.0±14.7、49.4±12.5,MYH:32.2±7.6비15.0±4.7、10.4±2.5,균P＜0.05);모형조여용제조간APE화MYH양성세포수비교차이균무통계학의의.결론 실험성대서대뇌피질경사후2주,VPN적DNA수복매APE화MYH수평명현하강,항양화제의포서람가명현승고기수평,종이조지수손세포사망.
Objective To investigate the damage within the ventroposterior nucleus (VPN) of the thalamus after focal cortical infarction and its mechanism, and explore the effect of ebselen on the oxidative damage after cerebral cortex infarction in hypertensive rats. Methods Middle cerebral artery occlusion (MCAO) was induced in stroke-prone renovascular hypertensive rats (RHRSP), and the rats were divided into four groups by table of random number: sham operation group, model group, vehicle group and ebselen group, each group consisted of 8 rats. In animals subjected to sham surgery the middle cerebral artery was exposed only. Ebselen (5 ml/kg) or vehicle (a mixed solvent consisting of 0. 5 % carboxymethyl cellulose and 0. 02% Tween 20, 5 ml/kg) was given by gastric gavage starting 24 hours after cerebral cortical infarction.Two weeks after the MCAO, the rats were sacrificed, and VPN from each group was sectioned and stained with hematoxylin-eosin (HE), and apurinic/apyrimidinic endonuclease (APE) and Escherichia coli Mut Y DNA glycosylase (MYH) were determined by immunohistochemistry. Results HE staining showed that ebselen ameliorated the VPN damage induced by ischemia. Immunohistochemical imaging analysis revealed a distinct nuclear staining of APE and nuclear and cytoplasm distribution of MYH in the entire region of the VPN. Compared with sham operation group, the number of APE and MYH positive cells decreased in model group and vehicle group (APE: 57.0±14.7, 49.4±12.5 vs. 101.0±13.6, MYH: 15.0±4.7, 10.4±2.5 vs. 56. 0± 13. 2, all P＜0.05). Compared with model group and vehicle group, the number of APE and MYH positive cells increased significantly in ebselen group (APE: 72. 2±7. 6 vs. 57. 0±14. 7, 49. 4±12. 5,MYH: 32. 2±7. 6 vs. 15.0±4.7, 10. 4±2.5, all P＜0. 05); the difference of the number of APE and MYH positive cells between model group and vehicle group showed no statistical significance. Conclusion After 2 weeks of MCAO, there is a marked decrease of APE and MYH in VPN; ebselen can obviously increase the level of APE and MYH, and ebselen may protect the VPN of the thalamus from damage after focal cortical infarction in rats.
