琼六糖对抗霉素A引起的肝细胞内间接氧化损伤的保护作用  

Inhibitory effect of agarohexaose on antimycin A induced generation of reactive oxygen species

作　　者：陈海敏[1] 马红辉[1] 严小军[1] 

机构地区：[1]宁波大学海洋生物工程重点实验室,浙江宁波315211

出　　处：《药学学报》2005年第10期903-907,共5页Acta Pharmaceutica Sinica

摘　　要：目的研究琼六糖对肝细胞的间接氧化损伤的保护作用。方法利用抗霉素A诱导肝细胞内的活性氧爆发,通过二乙酰基2,7-二氯荧光素(DCFH-DA)检测细胞内的氧化状况,利用荧光显微镜和流式细胞仪记录荧光变化情况,并对抗霉素A氧化所造成的细胞凋亡现象进行形态及TUNEL实验观测。结果琼六糖能够明显减少氧化细胞的数量及荧光强度。细胞凋亡研究结果发现,琼六糖能够改善细胞形态,降低由氧化所造成的细胞凋亡的出现。结论琼六糖能够有效地抑制肝细胞内活性氧的进一步爆发,并减少细胞的氧化损伤。Aim To evaluate the hepatocyte protective effect of agarohexaose against indirect oxidative stress injury induced by antimycin A. Methods Antimycin A was used to induce oxidative injury of human hepatocyte L-02. The oxidative degree in cells was detected by dichlorofluorescin diacetate （DCFH-DA） and the fluorescence generation was recorded by flow cytometer and fluorescent microscope. The apoptosis of L-02 cells induced by oxidation was identified by TUNEL test, and the morphologic features of cells were also observed. Results Agarohexaose at concentration of 1 mg · mL^-1 inhibited the oxidation of DCFH into DCF significantly. The fluorescence intensity and oxidized cell number decreased after the incubation with agarohexaose. The photomicrographs of antimycin A and agarohexaose treated cells revealed that agarohexaose could reduce the apoptotic morphologic features. The TUNEL results also indicated that the number of apoptotic cells decreased significantly after the treatment of agarohexaose. Conclusion Agarohexaose could inhibit the sudden increase reactive oxygen species （ROS） in cells significantly, and it also protected cells against oxidative stress injury in vitro.

关 键 词：琼六糖 氧化损伤 抗霉素A 细胞凋亡 

分 类 号：Q53[生物学—生物化学]