CAJ | 학술논문

目的观察银杏叶提取物(GBE)对大鼠局灶性脑缺血再灌注损伤的保护作用.方法将80只清洁雄性SD大鼠随机分为两组:对照组(A组,给予生理盐水治疗,n=40只),银杏叶提取物干预组(B组,给予等量的银杏叶提取物,n=40只),每组再分4个亚组,即再灌注后1、3、6、24h组,每个亚组10只.制作大鼠右侧大脑中动脉缺血再灌注模型.应用苏木素-伊红(HE)染色法观察脑组织形态病理学变化,应用酶联免疫吸附试验(ELISA)法检测胶质纤维相关蛋白(GFAP)在血清中的浓度变化；应用逆转录-聚合酶链反应(RT-PCR)法检测凋亡基因bax的表达.结果 HE染色:A组发现明显的梗死灶、神经细胞坏死、凋亡以及神经细胞外形难以辨认,大部分细胞结构消失.B组形态相对正常,损伤较A组轻.大鼠脑缺血再灌注损伤后GFAP的血清浓度升高,再灌注后各时间点(1、3、6、24h)B组GFAP的血清浓度(275.29±112.72、308.72±124.11、372.56±185.62、452.12±145.26) ng/L显著低于A组(437.17±152.26、490.27±198.37、583.45±201.42、656.26±256.36) ng/L(P＜0.05).RT-PCR检测显示bax mRNA表达水平在各时间点B组(0.256±0.018、0.302±0.023、0.417±0.034、0.527±0.052)显著低于A组(0.333±0.021、0.452±0.037、0.587±0.052、0.726±0.046) (P ＜0.05).结论 bax、GFAP在大鼠脑缺血再灌注后均发生明显的变化,参与大鼠脑缺血再灌注损伤的形成机制.银杏叶提取物可通过抑制GFAP的生成以及减少促凋亡基因bax的表达来减轻脑缺血再灌注损伤,从而对大鼠缺血脑组织具有显著保护作用.
목적 관찰은행협제취물(GBE)대대서국조성뇌결혈재관주손상적보호작용.방법 장80지청길웅성SD대서수궤분위량조:대조조(A조,급여생리염수치료,n=40지),은행협제취물간예조(B조,급여등량적은행협제취물,n=40지),매조재분4개아조,즉재관주후1、3、6、24h조,매개아조10지.제작대서우측대뇌중동맥결혈재관주모형.응용소목소-이홍(HE)염색법관찰뇌조직형태병이학변화,응용매련면역흡부시험(ELISA)법검측효질섬유상관단백(GFAP)재혈청중적농도변화；응용역전록-취합매련반응(RT-PCR)법검측조망기인bax적표체.결과 HE염색:A조발현명현적경사조、신경세포배사、조망이급신경세포외형난이변인,대부분세포결구소실.B조형태상대정상,손상교A조경.대서뇌결혈재관주손상후GFAP적혈청농도승고,재관주후각시간점(1、3、6、24h)B조GFAP적혈청농도(275.29±112.72、308.72±124.11、372.56±185.62、452.12±145.26) ng/L현저저우A조(437.17±152.26、490.27±198.37、583.45±201.42、656.26±256.36) ng/L(P＜0.05).RT-PCR검측현시bax mRNA표체수평재각시간점B조(0.256±0.018、0.302±0.023、0.417±0.034、0.527±0.052)현저저우A조(0.333±0.021、0.452±0.037、0.587±0.052、0.726±0.046) (P ＜0.05).결론 bax、GFAP재대서뇌결혈재관주후균발생명현적변화,삼여대서뇌결혈재관주손상적형성궤제.은행협제취물가통과억제GFAP적생성이급감소촉조망기인bax적표체래감경뇌결혈재관주손상,종이대대서결혈뇌조직구유현저보호작용.
Objective To explore the protective action of ginkgo biloba extract (GBE) after local cerebral ischemia and reperfusion in rats.Methods 80 male Sprague-Dawley rats were randomly divided into two groups:control group ( group A,saline injected,n =40 ),GBE intervention group ( group GBE injected,n =40),which were divided into 4 subgroups,namely,reperfusion after 1,3,6 and 24 h groups,10 in each subgroup.The animal model of right middle cerebral artery occlusion (MCAO) and reperfusion was established; pathological changes in brain morphology were observed by Hematoxylin and Eosin (HE) staining; serum glial fibrillary acidic protein (GFAP) was detected by enzyme linked immunosorbent assay (ELISA) method; changes of bax mRNA expression was detected by reverse transcriptionpolymerase chain reaction (RT-PCR) method.Results (1) Nerve cell necrosis,apoptosis were observed,neuronal shape was difficult to identify,and most of the cell structure disappeared in group A.While,the injury was milder at same time points in group B compared with group A.(2) ELISA results showed that serum GFAP levels increased after ischemia-reperfusion,the levels in group B (275.29 ±112.72,308.72 ± 124.11,372.56 ± 185.62,452.12 ± 145.26) ng/L were significantly lower than those in group A (437.17 ± 152.26,490.27 ± 198.37,583.45 ± 201.42,656.26 ± 256.36) ng/L,respectively( P ＜ 0.05 ).3.RT-PCR results showed that bax mRNA expression in group B (0.256 ± 0.018,0.302 ±0.023,0.417 ±0.034,0.527 ±0.052) was significantly higher than that in group A (0.333 ±0.021,0.452 ±0.037,0.587±0.052,0.726±0.046,respectively) (P＜0.05).Conclusion GFAP and bax change significantly after cerebral ischemia-reperfusion which may involve in cerebral isehemia reperfusion injury mechanism.GBE can significantly reduce the cerebral injury by down regulating the expression of GFAP and bax.GBE is effective on prevention of cerebral ischemia-reperfusion injury.