CAJ | 학술논문

目的探讨脑缺血再灌注损伤（I／R）大鼠丹红注射液干预后胶质原纤维酸性蛋白（GFAP）的表达变化。方法96只SD大鼠随机分为：正常对照8只（N组），不做任何处理；假手术组8只（S组），仅分离出血管，不做其他处理；缺血再灌注损伤组40只（I／R组），丹红注射液干预组40只（DI／R组），两组均采用大脑中动脉闭塞方法制作大鼠脑缺血再灌注模型。模型成功后，DI／R组从实验前一天开始腹腔注射丹红注射液（8 mL／kg ，Qd）；I／R组在相同时间点注射生理盐水。并于再灌注后6h、24h、48h、72h、7d的各时间点分批处死动物，免疫组织化学方法检测各组大鼠脑内GFAP的表达情况；各组大鼠在处死前行神经功能缺损评分。结果 N组和S组神经细胞中GFAP阳性细胞较少；I／R组缺血再灌注6 h GFAP的表达开始增加，72 h GFAP表达增加达到高峰，缺血再灌注7 d表达减少，DI／R组GFAP表达趋势同缺血再灌注组，但各时间点阳性细胞数明显低于I／R组（ P ＜0．05）；除6 h外的其余各时间点，DI／R组大鼠神经功能缺损均小于I／R组（ P ＜0．05），且DI／R组缺血再灌注时间越长，神经功能缺损程度越轻（ P＜0．05）。结论大鼠脑缺血再灌注损伤后，GFAP的表达上调，但丹红注射液下调GFAP的表达，抑制星形胶质细胞过度增生，减轻脑缺血后损伤。
목적탐토뇌결혈재관주손상（I／R）대서단홍주사액간예후효질원섬유산성단백（GFAP）적표체변화。방법96지SD대서수궤분위：정상대조8지（N조），불주임하처리；가수술조8지（S조），부분리출혈관，불주기타처리；결혈재관주손상조40지（I／R조），단홍주사액간예조40지（DI／R조），량조균채용대뇌중동맥폐새방법제작대서뇌결혈재관주모형。모형성공후，DI／R조종실험전일천개시복강주사단홍주사액（8 mL／kg ，Qd）；I／R조재상동시간점주사생리염수。병우재관주후6h、24h、48h、72h、7d적각시간점분비처사동물，면역조직화학방법검측각조대서뇌내GFAP적표체정황；각조대서재처사전행신경공능결손평분。결과 N조화S조신경세포중GFAP양성세포교소；I／R조결혈재관주6 h GFAP적표체개시증가，72 h GFAP표체증가체도고봉，결혈재관주7 d표체감소，DI／R조GFAP표체추세동결혈재관주조，단각시간점양성세포수명현저우I／R조（ P ＜0．05）；제6 h외적기여각시간점，DI／R조대서신경공능결손균소우I／R조（ P ＜0．05），차DI／R조결혈재관주시간월장，신경공능결손정도월경（ P＜0．05）。결론대서뇌결혈재관주손상후，GFAP적표체상조，단단홍주사액하조GFAP적표체，억제성형효질세포과도증생，감경뇌결혈후손상。
[Objective]To explore the effects of Danhong injection on the brain tissue expression of glial fibril‐lary acidic protein (GFAP) after cerebral ischemic reperfusion (IR) in rats .[Methods]A cerebral ischemia‐reperfu‐sion rat model was established through an occlusion of middle cerebral artery .A total of 96 healthy male Sprague‐Dawley rats were randomly divided into 4 groups of normal control ( n =8) ,sham operation ( n =8) ,ischemia reperfusion ( n =40) and Danhong injection ( n=40) .The expressions of GFAP in brain tissue were detected by immunohistochemistry at 6h ,24h ,48h ,72h and 7d post‐IR in ischemia‐reperfusion and Danhong intervention groups .Before sacrificing ,the neurological deficit scores were evaluated for all rats .The experimental results were analyzed with Spss17 .0 .[Results]The expressions of GFAP were weak in both normal control and sham op‐eration groups .And the levels of GFAP were evidently up‐regulated at 6h and peaked at 72h ( P <0 .05) .Then there was a gradual decline .Compared with ischemia/reperfusion group ,the levels of GFAP evidently decreased in Danhong intervention group ( P<0 .05) .At 24h ,48h ,72h and 7d ,the neurological deficit score of Danhong in‐tervention group was better than that of ischemia/reperfusion group .And the neurological deficit scores decreased in Danhong group ( P<0 .05) .[Conclusion]After ischemia‐reperfusion injury ,the levels of GFAP were evidently up‐regulated in ischemia‐reperfusion rats .Injury of brain tissue after ischemia‐reperfusion is blunted in Danhong intervention group .And Danhong may down‐regulate the level of GFAP and suppress the excessive proliferation of astrocytes .