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目的探讨营养组合物治疗再生障碍性贫血的作用机制。方法 BALB/c小鼠100只,适应性喂养1周后,随机分为:正常对照组、再障模型组(AA)及不同剂量的营养组合物组。采用皮下注射乙酰苯肼100mg/kg,次日X射线2.0Gy照射后,于试验第5天环磷酰胺80mg/kg腹腔注射,第15天重复以上步骤但不给予射线处理的方法建立再生障碍性贫血小鼠模型,以铅砖屏蔽施以假照射及单纯等量生理盐水相应部位注射为正常对照组。试验第7天开始,营养组合物高、中、低剂量组小鼠每天灌胃,分别给予1445.55,963.7,674.59mg/(kg·d)营养组合物,直至第45天,颈椎脱臼法处死小鼠,观察试验小鼠的骨髓象、透射电镜观察骨髓造血细胞、肝、脾、肾、脑细胞线粒体超微结构,流式细胞术检测线粒体跨膜电位。结果①透射电镜显示,再障模型组小鼠骨髓、肝、脾、肾细胞线粒体数目较正常对照组有不同程度明显减少(P<0.01),线粒体肿胀变性,呈空泡样变或髓样变,嵴不清楚或消失,内质网及核模有不同程度扩张。而各营养组合物组与再障模型组比较,此类细胞内线粒体数目明显增多,线粒体肿胀变性显著减轻。对照组小鼠肝、脾、肾、脑细胞线粒体结构无明显异常。②各营养组合物组骨髓、肝、脾、肾细胞随着营养组合物剂量的升高,线粒体膜电位明显升高,呈量效关系,抑制细胞的凋亡,而再障模型组细胞膜电位明显降低。结论 营养组合物能够明显改善AA小鼠骨髓、肝、脾、肾细胞线粒体数量和结构,抑制跨膜电位下降及细胞凋亡,此可能为其治疗AA的作用机制之一。
Objective To investigate the mechanism of nutritional composition in the treatment of aplastic anemia. Methods One hundred BALB / c mice were randomly divided into normal control group, AA group and different doses of nutritional composition group. Subcutaneous injection of acetophenhydrazine 100mg / kg, the next day 2.0Gy X-ray irradiation, the experimental day 5 days cyclophosphamide 80mg / kg intraperitoneal injection of the first 15 days to repeat the above steps but not given radiographic treatment to establish aplastic The model of anemia mice was treated with false exposure with lead-brick shield and injection of the same amount of normal saline into the normal control group. Beginning on the 7th day of experiment, the mice in high, middle and low dose of nutrition composition were given gavage daily and were given 1445.55, 963.7, and 674.59 mg / (kg · d) of nutritional composition respectively, until the 45th day, cervical dislocation Mice were observed, the bone marrow of mice were observed, the ultrastructure of hematopoietic cells, liver, spleen, kidney and brain were observed by transmission electron microscope. The mitochondrial transmembrane potential was detected by flow cytometry. Results ① The number of mitochondria in bone marrow, liver, spleen and kidney cells of mice with aplastic anemia was significantly lower than that of the normal control group (P <0.01) by transmission electron microscopy. The mitochondria were swollen and degenerated into vacuoles or myeloid metaplasia , Ridges unclear or disappear, endoplasmic reticulum and nuclear mode have different degrees of expansion. However, the number of mitochondria in each group was significantly higher than that in the aplastic anemia model group, and the mitochondrial swelling and degeneration was significantly reduced. The control group mice liver, spleen, kidney, brain mitochondrial structure no obvious abnormalities. ② The nutrition composition of the group of bone marrow, liver, spleen and kidney cells with the dose of nutritional composition increased mitochondrial membrane potential was significantly increased, the dose-response relationship, inhibition of cell apoptosis, while the cell membrane potential of aplastic anemia model group was significantly reduce. Conclusion The nutritional composition can significantly improve the quantity and structure of mitochondria in bone marrow, liver, spleen and kidney of AA mice, and inhibit the decrease of transmembrane potential and apoptosis, which may be one of its mechanisms of action in the treatment of AA.