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2.0Gy ^60Coγ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(100mg/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。
Objective To investigate the effect of polysaeehafides from Angelica sinensis (ASP3) on Bcl-2 and Bax protein expression of irradiated liver cells from mice. Methods Bel-2 and Bax protein expression of liver cells in vitro exposed to 2.0 Gy rays were examined by using immunohistoehemistry method. Results The expression of apoptosis-aeeelerating protein Bax in the irradiation group was enhanced obviously(70.83 % ), while apoptosis inhibiting protein Bel-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 expresslon(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 Bel-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.
出处
《中华放射医学与防护杂志》
CAS
CSCD
北大核心
2009年第5期476-478,482,共4页
Chinese Journal of Radiological Medicine and Protection
基金
山西省青年科研基金(2007021042)
关键词
当归
多糖
BCL-2
BAX
凋亡
辐射防护
Angelica sinensis
Polysaccharides
Bcl-2
Bax
Apoptosis
Radioprotection