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黄芪甲苷对高血压脑出血模型大鼠神经细胞凋亡及相关蛋白表达的影响
潘冬梅,田青,黄天韬,郭庆,马迎辉
0
(黄石市中心医院老年病科;黄石市中心医院神经外科)
摘要:
【摘要】 目的 探讨黄芪甲苷对高血压脑出血模型大鼠神经细胞凋亡及相关蛋白表达的影响。方法 50只SD大鼠随机分为5组:对照组(Ctrl组)、高血压脑出血模型组(HCH组)、黄芪甲苷治疗组(AST组) (10、20、50mg/kg),每组各5只。苏木素伊红(HE)染色观察脑组织病变。脱氧核糖核苷酸末端转移酶介导的缺口末端标记(TUNEL)染色检测细胞凋亡。实时定量PCR (qRTPCR)和蛋白印记分别检测Bax、Bcl2、Caspase3的mRNA水平和蛋白水平。酶联免疫吸附实验(ELISA)检测超氧化物歧化酶(SOD)、还原型谷胱甘肽(GSH)和丙二醛(MDA)水平。结果 高血压脑出血模型组大鼠神经行为缺陷评分高于对照组(P<0.01),与高血压脑出血模型组相比,黄芪甲苷治疗(10、20、50 mg/kg)组大鼠神经行为缺陷评分下降(P<0.01),且随着黄芪甲苷浓度的增加,大鼠神经行为缺陷评分逐渐降低(P< 0.01)。高血压脑出血模型组大鼠脑组织细胞凋亡高于对照组(P< 0.01),与高血压脑出血模型组相比,黄芪甲苷治疗(10、20、50 mg/kg)组大鼠脑组织细胞凋亡降低(P< 001),且随着黄芪甲苷浓度的增加,大鼠脑组织细胞凋亡则逐渐降低(P<0.01)。与对照组相比,高血压脑出血模型组大鼠Bax和Caspase3的mRNA水平和蛋白水平上升,Bcl2 的mRNA水平和蛋白水平下降(P<0.01),与高血压脑出血模型组相比,黄芪甲苷治疗(10、20、50 mg/kg)组大鼠Bax和Caspase3的mRNA水平和蛋白水平逐渐降低,Bcl2 的mRNA水平和蛋白水平逐渐升高(P<0.01)。与对照组相比,高血压脑出血模型组大鼠SOD和GSH水平降低,MDA水平上升(P<0.01),与高血压脑出血模型组相比,黄芪甲苷治疗(10、20、50 mg/kg)组大鼠SOD和GSH水平逐渐升高,MDA水平逐渐下降(P<0.01)。结论 黄芪甲苷以浓度依赖性的方式通过抑制氧化应激减轻高血压脑出血模型大鼠神经行为学缺陷,缓解脑组织病变,减轻脑细胞凋亡。
关键词:  高血压脑出血  黄芪甲苷  脑损伤  细胞凋亡  氧化应激
DOI:
基金项目:湖北省卫生和计划生育委员会科研项目
The effects of astragaloside IV on the neuronal apoptosis and expression of ralated proteins in hypertensive cerebral
PAN Dongmei,TIAN Qing,HUANG Tiantao,GUO Qing,MA Yinghui
(Department of Geriatrics, Huangshi Central Hospital)
Abstract:
【Abstract】 Oojective To explore the effects of astragaloside IV on the neuronal apoptosis and expression of related proteins in hypertensive cerebral hemorrhage model rats. Methods 50 rats were randomly divided into healthy control group (Ctrl), hypertensive cerebral hemorrhage model group (HCH) and astragaloside IV treatment groups (AST (10, 20, 50 mg/kg)). The pathological changes of brain tissues were observed by hematoxylineosin (HE) staining. The apoptosis of brain tissues was detected by terminal deoxynucleotidyl transferase mediated dUTP nick labeling (TUNEL) staining. The mRNA and protein levels of Bax, Bcl2 and Caspase3 were measured by quantitative realtime reverse transcription PCR (qRTPCR) and western blot. The levels of superoxide dismutase (SOD), glutathione (GSH) and malondialdehyde (MDA) were tested by enzymelinked immunosorbent assay (ELISA). Results The neural deficit scores in HCH group were higher than that of control group (P< 0.01). Compared with HCH group, the neural deficit scores in AST (10, 20, 50 mg/kg) groups were reduced (P<0.01). Furthermore, the neurobehavioral deficit score was decreased gradually with the increase of astragaloside concentration (P<001). The pathological changes of brain tissues of hypertensive cerebral hemorrhage rats were relieved. The apoptosis of brain tissues in HCH group was higher than control group (P<0.01). Compared with HCH group, the apoptosis of brain tissues in AST (10, 20, 50 mg/kg) groups was alleviated (P < 0.01). Moreover, apoptosis of brain tissue was reduced gradually with the increase of astragaloside concentration (P<0.01). Compared with control group, the mRNA and protein levels of Bax and Caspase3 in HCH group were increased with declined levels of Bcl2 (P<0.01). Compared with HCH group, the mRNA and protein levels of Bax and Caspase3 in AST (10, 20, 50 mg/kg) groups were attenuated with enhancive levels of Bcl2 (P < 0.01). Compared with control group, the levels of SOD and GSH in HCH group were decreased wirh elevated levels of MDA (P < 0.01). Compared with HCH group, the levels of SOD and GSH in AST (10, 20, 50 mg/kg) groups were enhanced with reduced levels of MDA (P<0.01). Conclusion Astragaloside IV alleviates the neurobehavioral deficits, pathological changes of brain tissues and apoptosis in hypertensive cerebral hemorrhage model rats by inhibiting oxidative stress in a concentrationdependent manner.
Key words:  Hypertensive cerebral hemorrhage  Astragaloside IV  Brain injury  Apoptosis  Oxidative stress

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