孙元琳,汤坚,顾小红,等.当归多糖对小鼠肝细胞辐照后Bcl-2和Bax蛋白表达的影响[J].中华放射医学与防护杂志,2009,29(5):476-478,482.SUN Yuan-lin,TANG Jian,GU Xiao-hong,et al.Effect of polysaccharides from Angelica sinensis on Bcl-2 and Bax protein expression of irradiated liver cells[J].Chin J Radiol Med Prot,2009,29(5):476-478,482 |
当归多糖对小鼠肝细胞辐照后Bcl-2和Bax蛋白表达的影响 |
Effect of polysaccharides from Angelica sinensis on Bcl-2 and Bax protein expression of irradiated liver cells |
投稿时间:2008-11-11 |
DOI: |
中文关键词: 当归 多糖 Bcl-2 Bax 凋亡 辐射防护 |
英文关键词:Angelica sinensis Polysaccharides Bcl-2 Bax Apoptosis Radioprotection |
基金项目:山西省青年科研基金(2007021042) |
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中文摘要: |
目的 探讨当归多糖ASP3对小鼠肝细胞培养液辐照后凋亡相关基因bcl-2和bax的蛋白表达的影响。方法 以当归多糖的自制提取物ASP3为受试物,用2.0 Gy 60Co γ射线照射小鼠肝细胞。采用免疫组织化学方法,检测辐射损伤诱发的肝细胞凋亡相关基因bcl-2和bax的蛋白表达。结果 辐射对照组的Bcl-2蛋白表达阳性减弱(55.60%),Bax表达明显增多(70.83%),与正常对照组比较,差异有统计学意义(P<0.01)。当归多糖ASP3能够调节辐照肝细胞Bcl-2家族蛋白的表达,即抑制Bax的高表达(64.14%/58.37%),同时提高Bcl-2的表达量(59.21%/67.45%),且高剂量(100 mg/L)ASP3组与辐射对照组比较,差异有统计学意义(P<0.05)。结论 当归多糖ASP3对辐射诱导的肝细胞凋亡有抑制作用,并通过提高Bcl-2/Bax比值减少细胞凋亡的发生,进而提高肝细胞的DNA损伤修复能力和辐射耐受性。 |
英文摘要: |
Objective To investigate the effect of polysaccharides from Angelica sinensis (ASP3) on Bcl-2 and Bax protein expression of irradiated liver cells from mice. Methods Bcl-2 and Bax protein expression of liver cells in vitro exposed to 2.0 Gy rays were examined by using immunohistochemistry method. Results The expression of apoptosis-accelerating protein Bax in the irradiation group was enhanced obviously(70.83%),while apoptosis inhibiting protein Bcl-2 tended to decline(55.60%),with the statistically significant difference(P<0.01) compared with that of the control. ASP3 pretreatment could regulate Bcl-2 and Bax protein expression of liver cells,inhibiting Bax protein expression(64.14/58.37%) and increasing Bcl-2 protein expression(59.21%/67.45%).The differences between the high dosage(100 mg/L of ASP3) and the irradiation group were statistically significant(P<0.05). Conclusions ASP3 pretreatment could prohibit the apoptosis of radiation-damaged liver cells due to abnormal expression of Bcl-2 and Bax, and reduce the cell apoptosis by increasing Bcl-2/Bax protein expression so as to enhance the radiation endurance of liver cells. |
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