扇贝多肽对^60Coγ射线辐射损伤小鼠胸腺淋巴细胞的保护机制研究

Protective effect of polypeptides from Chlamys farreri on murine thymocytes damaged by ^60 Co γ-rays

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.