摘要
目的探讨在^60Coγ射线单次照射下,扇贝多肽(PCF)对小鼠胸腺淋巴细胞辐射损伤的保护机制。方法实验细胞分为6组:对照组、^60Co模型组、^60Co+0.125%PCF组、^60Co+0.25%PCF组、^60Co+0.5%PCF组和^60Co+0.1%VitC组。除对照组外,其他5组均照射2Gy,分别检测细胞活性;胞质谷胱甘肽过氧化物酶(GSH—Px)、活性氧(ROS)含量以及细胞抗超氧阴离子能力(A-SAC)和总抗氧化能力(T-AOC);线粒体膜电位(△ψM);细胞p53、Bcl-2、Bax基因蛋白的表达。结果PCF能提高小鼠胸腺淋巴细胞的活性;提高细胞质GSH—Px的活性,降低ROS含量,提高A-SAC及T-AOC;稳定线粒体的膜电位;抑制^60Co辐射后小鼠胸腺淋巴细胞p53基因蛋白和Bax蛋白在胞质的表达,增强Bcl-2蛋白的表达。以上结果差异均有统计学意义(P〈0.05)。结论扇贝多肽能提高体外培养的小鼠胸腺淋巴细胞的活性,抑制^60Coγ照射诱导的淋巴细胞凋亡,对^60Co辐射损伤的小鼠胸腺淋巴细胞具有保护作用。
Objective To study the effect and mechanism of polypeptide from Chlamysfarreri(PCF) on the thymocytes damaged by ^60Co γ-rays. Methods The ceils were randomly divided into six groups: control group, ^60Co groups (2 Gy, model), ^60Co + 0.5% PCF, ^60Co + 0.25% PCF, ^60Co + 0.125% PCF, ^60Co + 0.1% VitC. The concentration of GSH-Px, ROS, A-SAC, T-AOC and the cells' viability were determined. The mitochondria membrane potential were tested. The expressions of P53, Bax and Bcl-2 proteins were examined. Results The activities of GSH-Px, A-SAC, T-AOC in cells were enhanced, and the amounts of ROS were decreased by PCF. The expression of Bcl-2 gene was up-regulated, and down-regulated for the expression of P53 and Bax. All observed indexes of the PCF groups were significantly different compared with model group ( P 〈 0.05). Conclusions PCF has the protective effects on damages of thymocytes caused by ^60Co irradiation. The mechanisms might be related to inhibiting of lymphocyte apoptosis and enhancing the activities of lymphocytes.
出处
《中华放射医学与防护杂志》
CAS
CSCD
北大核心
2008年第6期618-620,共3页
Chinese Journal of Radiological Medicine and Protection