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目的:探讨去甲斑蝥素(NCTD)对环磷酰胺(CTX)诱导的低白细胞模型大鼠骨髓粒-单集落刺激因子(GM-CSF)表达的影响。方法:将90只SD大鼠随机分为模型对照组、空白对照组、NCTD高剂量组、NCTD低剂量组和升白药物对照组;采用腹腔注射CTX(30mg/㎏)方法复制低白细胞大鼠模型后,各药物对照组及空白对照组分别以一定浓度药物、双蒸水灌胃,并于灌胃后第3、6、9天采集外周血及骨髓组织样本进行以下指标检测:(1)全自动血细胞分析仪检测外周血WBC数量;(2)酶联免疫双抗夹心法(ELISA)检测外周血GM-CSF含量;(3)采用免疫组化(IHC)方法检测骨髓组织细胞中GM-CSF的表达。结果:(1)与空白对照组比较,CTX处理后各实验组大鼠白细胞数量显著降低(P<0.05);(2)在CTX诱导的低白细胞模型大鼠中,NCTD高、低剂量组和升白药物对照组外周血WBC显著升高(P<0.05),且GM-CSF在骨髓组织细胞中的表达显著增高(P<0.05),其在外周血中的含量也有增加趋势。结论:NCTD可以显著升高CTX处理后SD大鼠外周血白细胞数量,其机制可能与NCTD上调GM-CSF的表达有关。
AIM: To investigate the effects of norcantharidin (NCTD) on the expression of granulocyte-monocyte colony stimulating factor (GM-CSF) in low leukocyte induced by cyclophosphamide (CTX) in rats. Methods: Ninety Sprague-Dawley rats were randomly divided into model control group, blank control group, NCTD high dose group, NCTD low dose group and lightening drug control group; low-leukocyte rats were induced by intraperitoneal injection of CTX (30mg / kg) After the model, each drug control group and blank control group were given a certain concentration of drugs, double distilled water gavage, and 3, 6, 9 days after gavage peripheral blood and bone marrow samples were collected for the following indicators: (1) (2) Enzyme-linked immunosorbent assay (ELISA) was used to detect the content of GM-CSF in peripheral blood; (3) Immunohistochemistry (IHC) was used to detect the number of WBC in peripheral blood; CSF expression. Results: (1) Compared with the blank control group, the number of leukocytes in the experimental groups after CTX treatment was significantly decreased (P <0.05); (2) In CTX-induced low leukocyte model rats, NCTD high and low dose groups The WBC of peripheral blood of ascending ailments control group was significantly increased (P <0.05), and the expression of GM-CSF in bone marrow cells was significantly increased (P <0.05), and its content in peripheral blood also increased. Conclusion: NCTD can significantly increase the number of peripheral blood leukocytes in CTX-treated SD rats, which may be related to the up-regulation of GM-CSF expression by NCTD.