CAJ | 학술논문

目的观察虾青素在大鼠蛛网膜下腔出血(SAH)后早期脑损伤(EBI)中的保护作用.方法成年雄性SD大鼠72只,随机分为假手术组(sham)、SAH加安慰剂组(vehicle)和虾青素处理组(ATX).通过建立大鼠视交叉SAH模型,于手术后24 h分别检测大鼠脑组织含水量、伊文氏蓝含量的改变,并应用Western blot技术、原位末端转移酶标记(TUNEL)以及分光光度比色法分别检测脑组织中半胱氨酰天冬氨酸特异性蛋白酶(Caspase)-3蛋白水平的表达、神经细胞凋亡和脑组织丙二醛(MDA)、谷胱甘肽(GSH)及超氧化物歧化酶(SOD)的变化.结果 SAH后24 h大鼠脑组织含水量[(80.76±0.67)％]、血脑屏障通透性[(2.17 ±0.53)μg/g]显著升高;颞叶底部皮层Caspase-3蛋白水平表达(0.49 ±0.13)和TUNEL凋亡阳性细胞[(41.54±9.38)％]也明显增多;应用虾青素干预以后,大鼠脑组织含水量[(79.91±0.42)％]、血脑屏障通透性[(1.35 ±0.46) μg/g]、Caspase-3蛋白水平表达(0.34±0.06)和TUNEL凋亡阳性细胞[(27.86±5.17)％]均显著减少,同时,虾青素能够减轻SAH后的氧化应激损伤[MDA:(2.52±0.60)、(4.44±1.32)、(2.64±0.78) nmol/mg;GSH:(6.50±1.80)、(3.72±1.12)、(6.23±0.87)μmol/g;SOD:(25.71 ±4.00)、(14.71 ±2.35)、(21.61±3.87) U/mg].结论虾青素能够减轻SAH后EBI,并可能与其强抗氧化性有关.
목적 관찰하청소재대서주망막하강출혈(SAH)후조기뇌손상(EBI)중적보호작용.방법 성년웅성SD대서72지,수궤분위가수술조(sham)、SAH가안위제조(vehicle)화하청소처리조(ATX).통과건립대서시교차SAH모형,우수술후24 h분별검측대서뇌조직함수량、이문씨람함량적개변,병응용Western blot기술、원위말단전이매표기(TUNEL)이급분광광도비색법분별검측뇌조직중반광안선천동안산특이성단백매(Caspase)-3단백수평적표체、신경세포조망화뇌조직병이철(MDA)、곡광감태(GSH)급초양화물기화매(SOD)적변화.결과 SAH후24 h대서뇌조직함수량[(80.76±0.67)％]、혈뇌병장통투성[(2.17 ±0.53)μg/g]현저승고;섭협저부피층Caspase-3단백수평표체(0.49 ±0.13)화TUNEL조망양성세포[(41.54±9.38)％]야명현증다;응용하청소간예이후,대서뇌조직함수량[(79.91±0.42)％]、혈뇌병장통투성[(1.35 ±0.46) μg/g]、Caspase-3단백수평표체(0.34±0.06)화TUNEL조망양성세포[(27.86±5.17)％]균현저감소,동시,하청소능구감경SAH후적양화응격손상[MDA:(2.52±0.60)、(4.44±1.32)、(2.64±0.78) nmol/mg;GSH:(6.50±1.80)、(3.72±1.12)、(6.23±0.87)μmol/g;SOD:(25.71 ±4.00)、(14.71 ±2.35)、(21.61±3.87) U/mg].결론 하청소능구감경SAH후EBI,병가능여기강항양화성유관.
Objective To study the effects of astaxanthin (ATX) on the early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH) in rats.Methods A total of 72 male SD rats were randomly divided into three groups:sham group,SAH + vehicle group and SAH + ATX group.The prechiasmatic cistern SAH rat model was established in this experiment.Brain edema and Evans blue extravasation were measured at 24 h after surgery.The levels of Caspase-3,apoptotic index and malondialdehyde (MDA),glutathione (GSH),and superoxide dismutase (SOD) in the brain cortex were evaluated by Western blotting,terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining,and spectrophotometric method,respectively.Results The brain edema [(80.76 ± 0.67) ％] and blood-brain barrier permeability [(2.17 ±0.53) μg/g] were significantly aggravated at 24 h after SAH.In addition,the levels of Caspase-3 expression [(0.49 ± 0.13)] and neural cell apoptosis [(41.54 ±9.38) ％] were increased in the inferior basal temporal lobe followomh SAH.After ATX administration,the brain edema [(79.91 ± 0.42) ％],BBB disruption [(1.35 ± 0.46) μg/g],Caspase-3 levels [(0.34 ± 0.06)] and neural cell apoptosis [(27.86 ± 5.17) ％] were ameliorated after SAH.Meanwhile,ATX could attenuate the oxidative stress injury [(MDA:2.52 ± 0.60,4.44 ± 1.32 and 2.64 ±0.78); (GSH:6.50±1.80,3.72±1.12 and 6.23 ±0.87); (SOD:25.71 ±4.00,14.71 ±2.35 and 21.61 ± 3.87)] in brain cortex after SAH.Conclusion ATX could alleviate EBI after SAH by its powerful anti-oxidant property.