CAJ | 학술논문

目的观察丙二醛(MDA)和内皮型一氧化氮合酶(eNOS)在局灶性脑梗死大鼠的动态表达及丁苯酞干预效应.方法将54只雄性SD大鼠随机分为假手术组、模型组、治疗组.每组再分为3个亚组:1d组、3d组和7d组,每亚组6只.模型组和治疗组采用线栓法制作大鼠大脑中动脉闭塞模型(MCAO),假手术组只分离不结扎.治疗组在大鼠苏醒后以丁苯酞植物油灌胃,假手术组和模型组同法给予等量植物油灌胃.应用硫代巴比妥酸(TBA)法检测脑组织MDA含量,Western blot检测脑组织eNOS表达,并对两者进行相关分析.结果 MDA含量随时间延长从12.005±0.608(模型组)逐渐降至7.315±0.404(模型组).各时间点模型组12.005 ±0.608(1 d)较治疗组9.323±0.727(1 d)增高;治疗组9.323 ±0.727(1 d)较假手术组4.043 ±0.274(1 d)增高.差异均有统计学意义(P＜0.05).eNOS含量随时间延长从0.136 ±0.009(模型组)逐渐增加至0.241 ±0.012(模型组);各时间点模型组0.136±0.009(1 d)较假手术组0.101 ±0.012(1 d)增高,治疗组0.199±0.010(1 d)较模型组0.136 ±0.009(1 d)增高,差异均有统计学意义(P＜0.05).且MDA含量和eNOS表达呈负相关(P＜0.05).结论丁苯酞通过减少脑缺血大鼠氧化应激损伤及eNOS脱耦联,发挥神经保护作用,且MDA和eNOS呈负相关.
목적 관찰병이철(MDA)화내피형일양화담합매(eNOS)재국조성뇌경사대서적동태표체급정분태간예효응.방법 장54지웅성SD대서수궤분위가수술조、모형조、치료조.매조재분위3개아조:1d조、3d조화7d조,매아조6지.모형조화치료조채용선전법제작대서대뇌중동맥폐새모형(MCAO),가수술조지분리불결찰.치료조재대서소성후이정분태식물유관위,가수술조화모형조동법급여등량식물유관위.응용류대파비타산(TBA)법검측뇌조직MDA함량,Western blot검측뇌조직eNOS표체,병대량자진행상관분석.결과 MDA함량수시간연장종12.005±0.608(모형조)축점강지7.315±0.404(모형조).각시간점모형조12.005 ±0.608(1 d)교치료조9.323±0.727(1 d)증고;치료조9.323 ±0.727(1 d)교가수술조4.043 ±0.274(1 d)증고.차이균유통계학의의(P＜0.05).eNOS함량수시간연장종0.136 ±0.009(모형조)축점증가지0.241 ±0.012(모형조);각시간점모형조0.136±0.009(1 d)교가수술조0.101 ±0.012(1 d)증고,치료조0.199±0.010(1 d)교모형조0.136 ±0.009(1 d)증고,차이균유통계학의의(P＜0.05).차MDA함량화eNOS표체정부상관(P＜0.05).결론 정분태통과감소뇌결혈대서양화응격손상급eNOS탈우련,발휘신경보호작용,차MDA화eNOS정부상관.
Objective To investigate the expression of malondialdehyde (MDA) and endothelial nitrioxide synthase (eNOS) in ratwith focal cerebral ischemi(FCI) and the effectof butylphthalide (NBP) conditioning.MethodMale SD rat(n =54) were randomly divided into three groups: sham, model and NBP-treated groups, and each group wadivided into three subgroups: 1 sday group, 3rd day group and 7th day group (n =6 each).The ramiddle cerebral artery occlusion (MCAO) model waestablished in model and NBP-treated groupby intraluminal suture technique, and sham group wajusgiven separation of the blood vessels.NBP-Treated group wagiven NBP vegetable oil by intragastriadministration afterecovery from anaesthesia, and sham and model groupgiven the same dose of vegetable oil.TBmethod waused to measure MDcontent, and Western blotting to detecthe level of eNOin brain tissue.Correlation analysiwacarried on the MDcontenand level of eNOS.ResultWith the extension MDcontenwagradually decreased from 12.005 ±0.608 to 7.315 ±0.404 in model group.The MDcontenin model group a1sday (12.005 ±0.608) wahighethan in NBP-treated group a1sday (9.323 ±0.727), and thain NBP-treated group a1sday wahighethan in sham group a1sday (4.043 ±0.274).The differencewere all statistically significan(P ＜ 0.05).With the extension eNOwagradually increased from 0.136 ±0.009 to 0.241 ±0.012 in model group.eNOin model group a1sday (0.136 ±0.009) wahighethan in sham group a1sday (0.101 ±0.012), and the in NBP-treated group a1sday (0.199 ±0.010) wahighethan in model group a1sday.The differencewere all statistically significan(P ＜ 0.05).The MDcontenand eNOlevel had negative correlation.Conclusion NBP may play neuroprotective effecby ameliorating oxidative stresinjury and eNOdecoupling on cerebral ischemirats.MDcontenand eNOlevel show negative correlation.