论文部分内容阅读
目的考察番石榴酸(guavenoic acid,GA)对INS-1胰岛β细胞氧化损伤的作用。方法培养INS-1胰岛β细胞,给予番石榴酸0.3、1、3、10、30 nmol·L-1,并设空白对照组、溶媒对照组及阳性药组,药物作用时间均为48 h。650μmol·L-1H2O2干预细胞2 h建立氧化损伤模型,用四甲基偶氮唑蓝法检测药物对INS-1β细胞氧化损伤的保护作用,用核染色法观察细胞核变化,用流式细胞术检测药物对细胞活性氧生成的作用,用双染-流式细胞术检测药物对细胞凋亡的保护作用。结果与氧化损伤模型组比较,低剂量的番石榴酸(0.3、1 nmol·L-1)能显著保护INS-1β细胞活力(P<0.05或P<0.01);核染色结果显示,与氧化损伤模型组相比,低浓度番石榴酸(0.3 nmol·L-1)作用下,细胞荧光强度较弱。0.3、1、3 nmol·L-1番石榴酸均能十分显著地降低二氯荧光黄(DCF)荧光强度(P<0.01),即减少细胞内活性氧的产生。0.3 nmol·L-1番石榴酸能显著抵抗细胞凋亡的发生(P<0.05)。结论番石榴酸能对抗INS-1细胞氧化损伤,可能与其抑制细胞内活性氧的产生、对抗细胞凋亡有关。
Objective To investigate the effect of guavenoic acid (GA) on the oxidative damage of INS-1 pancreatic islet β cells. Methods INS-1 islet β cells were cultured and guaiadic acid was administered at 0.3, 1, 3, 10, 30 nmol·L-1. The blank control group, vehicle control group and positive drug group were used. The drug action time was 48 h. The cells were treated with 650μmol·L-1H2O2 for 2 hours to establish the oxidative damage model. The protective effect of the drug on the oxidative damage of INS-1β cells was detected by MTT assay. The nuclear changes were observed by nuclear staining and detected by flow cytometry. The effect of the drug on the generation of reactive oxygen species in the cells was examined by double staining-flow cytometry to determine the protective effect of the drug on apoptosis. Results Compared with the oxidative injury model group, low dose guavadic acid (0.3, 1 nmol·L-1) could significantly protect the viability of INS-1β cells (P<0.05 or P<0.01); nuclear staining results showed that the oxidative damage Compared with the model group, the fluorescence intensity of the cells was weak under the effect of low concentration guavadic acid (0.3 nmol·L-1). 0.3,1,3 nmol·L-1 guavalic acid could significantly reduce the fluorescence intensity of dichlorofluorescein yellow (DCF) (P<0.01), which means that the production of reactive oxygen species in cells was reduced. 0.3 nmol·L-1 guavaic acid could significantly resist the occurrence of apoptosis (P<0.05). Conclusion Guavaic acid can counteract the oxidative damage of INS-1 cells, which may be related to its inhibition of intracellular reactive oxygen species production and anti-apoptosis.