摘要
为了证实当归多糖可以通过调控线粒体膜稳定性干预鼠再障模型设计了该实验。ICR小鼠随机分为对照组、再障组和当归多糖治疗组。其中再障小鼠使用60Coγ照射和腹腔注射环磷酰胺和环孢素的方法造模。对照组小鼠采用铅屏蔽照射。对照组和再障组小鼠使用生理盐水腹腔注射,治疗组小鼠口服当归多糖两周。分别检测骨髓单个核细胞的线粒体超微结构和膜电位。检测COX、MDH在三组中的寒凉差异。结果显示,再障组中线粒体数量和膜电位较对照组均有显著下降,应用当归多糖干预后,有不同程度的回升。治疗组的线粒体裂解时间较再障组大幅延迟(P<0.05)。我们认为当归多糖可以提升再障骨髓单个核细胞的线粒体膜稳定性,并可能抑制线粒体通路的凋亡。
In order to investigate the mechanism of mitochondrial membrane stabilization by Angelica sinensis polysaccharide (ASP) in murine aplastic anemia (AA).ICR mice were randomly divided into control, AA and ASP-treated groups. The AA group mice were treated with 60Coγand intraperitoneal injections of cyclophosphamide and chloramphenicol. The control animals were treated with lead shielding irradiation and saline injection. The treated AA mice were fed with ASP for 2 wk. Mitochondrial ultrastructure of the bone marrow was observed by transmission electron microscopy, and the transmembrane potential of bone marrow-nucleated cells (BMNC)was examined by fluorescence spectrophotometry. The Cox and MDH contents of the medium were also studied in the three groups.The mitochondrial number and transmembrane potential of BMNC in the bone marrow decreased in the AA group as compared to the control group, but improved in the ASP-treated group as compared to the AA group. Complete mitochondrial cleavage in the ASP-treated group was significantly delayed (P<0.05) as compared to the AA group. We conclude that ASP might improve mitochondrial membrane stabilization, and suppress the downregulation of transmembrane potential and apoptosis of BMNC in AA.
基金
the National Natural Science Foundation of China (No. 81202839)
the National Natural Science Foundation of China (No. 81774080)
the “Taishan Scholar” Project Special Fund
the Study Abroad Funding by the Shandong health science and technology association and the Affiliated Hospital of Shandong University of Traditional Chinese Medicine.
关键词
再生障碍性贫血
当归多糖
线粒体
膜电位
ICR小鼠
aplastic anemia
Angelica sinensis polysaccharide
mitochondria
membrane potential
ICR mice
