文献类型：期刊文献

中文题名：党参多糖对小鼠造血干细胞衰老相关蛋白p53 p21 Bax和Bcl-2的影响

英文题名：Effect of Codonopsis Polysaceharide on Protein Expression of p53 p21 Bax and Bcl-2 Associated with Aging of Hematopoietic Stem Cells in Mice

作者：李义波[1];杨柏龄[2];侯茜[1];谢荣丹[1];张帆[1]

第一作者：李义波

机构：[1]甘肃中医药大学甘肃省高校重大疾病分子医学与中医药防治研究重点实验室,甘肃兰州730000;[2]武警森林指挥部机动支队卫生队,北京102202

第一机构：甘肃中医药大学科研实验中心（甘肃省中医药标准化技术委员会秘书处）

年份：2017

卷号：33

期号：2

起止页码：120

中文期刊名：解放军药学学报

外文期刊名：Pharmaceutical Journal of Chinese People's Liberation Army

收录：CSTPCD;;CSCD:【CSCD_E2017_2018】；

基金：2016年甘肃省高等学校科研项目;No.2016A-043

语种：中文

中文关键词：党参多糖;造血干细胞;细胞衰老

外文关键词：codonopsis polysaceharides;hematopoietic stem cell;cell aging

摘要：目的研究党参多糖对辐射所致小鼠造血干细胞中p53、p21、Bax、Bcl-2蛋白表达的影响以及延缓造血干细胞衰老的可能机制。方法将C57BL/6J小鼠使用随机数字表法分成空白组、模型组和党参多糖低、中、高剂量组。模型组和党参多糖各组采用3Gy/8F强度的X射线均匀照射小鼠,建立造血干细胞衰老模型。党参多糖各组在照射期间分别给小鼠灌胃党参多糖100、200、300mg·kg^(-1),空白组、模型组给予等量生理氯化钠溶液。采用免疫磁珠分离造血干细胞,并检测各组细胞周期变化。用β-半乳糖苷酶染色验证小鼠造血干细胞衰老模型是否成功,用免疫印迹法检测造血干细胞p21、p53、Bax和Bcl-2蛋白表达。结果模型组比其他各组造血干细胞G1期阻滞明显增加(P<0.05);模型组β-半乳糖苷酶染色阳性细胞率明显高于正常组(P<0.05),p53、p21、Bax蛋白表达上调(P<0.05),Bcl-2蛋白表达下调(P<0.05)。党参多糖各组比模型组造血干细胞G1期阻滞明显降低(P<0.05),β-半乳糖苷酶染色阳性率明显低于模型组(P<0.05),p53、p21、Bax蛋白表达下调(P<0.05)、Bcl-2蛋白表达上调(P<0.05)。结论党参多糖能够延缓X线诱导的造血干细胞衰老,其作用机制可能与p53-p21信号通路,Bax与Bcl-2凋亡途径有关。
Objective To study the effect of Codonopsis polysaccharide （CPPS） on the protein expres sion of p53, p21, Bax and Bcl-2 in hematopoietic stem cells （HSC） induced by radiation,and to investigate the possible mechanism by which CPPS delays the aging of HSC.Methods The C57BL/6J mice were randomly divided into blank, model and CPPS low, medium and high groups using the random number table method. The model group and CPPS groups were irradiated with X rays of 3Gy/8F,so as to establish the HSC aging model. CPPS groups were respectively given CPPS 100, 200 and 300 mg·kg^-1 during irradiation.The blank group and model group were given an equal volume of normal saline （NS）. Immunomagnetic beads method was used for separation and each cell was tested for their cycle changes. Beta-galactosidase （SA-beta-Gal） staining was used to verify the success of HSC aging model in mice.The expression of p21, p53, Bax and Bcl-2 protein in HSC was detected by Western blot. Results Compared with other groups, HSC G1 arrest in the model group was significantly increased （ P〈0.05）. The positive cell rate of SA-be- ta-Gal in model group was significantly higher than that in normal group （ P 〈0.05）,the protein expression of p53, p21, Bax was up-regulated（ P 〈0.05） and the expression of Bcl-2 protein was down-regulated （ P 〈0.05）.HSC G1 arrest in CPPS groups was significantly lower （ P 〈0.05） than that in the model group.The positive cell rates of SA-beta-Gal in CPPS group was significantly lower than that of model group （ P 〈0.05）, the expression of p53, p21 and Bax was down-regulated （ P 〈0.05）, and the expression of Bcl-2 protein was up-regulated （ P〈0.05）.Conclusion CPPS can delay the aging of HSC induced by X-ray.The mechanism may be related to the signaling pathway of p53-p21 , the apoptosis pathway of Bax and Bcl-2.