中文摘要：

目的：观察马齿苋多糖组分（POP I）对四氧嘧啶致大鼠胰岛素瘤细胞（INS-1 cell line）氧化损伤的影响.方法：不同浓度POP I （0.05,0.1,0.5,1.0,2.0,5.0和10.0 mg/mL）作用四氧嘧啶氧化损伤的INS-1细胞1d、3d和5d后,分别测定其细胞存活率、胰岛素分泌量、超氧化物歧化酶（SOD）活性、丙二醛（MDA）含量和谷胱甘肽（GSH）含量.结果：POP I可明显抑制由四氧嘧啶所致的INS-1细胞存活率降低、SOD活性下降、GSH浓度减少和.MDA含量增加,并存在时-效和量-效关系;在5.6 mmol/L或16.7 mmol/L葡萄糖刺激下,POP I浓度依赖性地促进了INS-1细胞分泌胰岛素.结论：一定浓度范围内,POPI对四氧嘧啶致胰岛β细胞损伤有明显的保护作用,其作用机理可能与POP I提高细胞抗氧化能力有关.

英文摘要：

the paper aims to investigate the inhibitive effects of polysaccharides from Portulaca oleracea L. （POP I） on alloxan-induced INS-1 cells damage. Methods： POP I at Various concentrations （0.05,0.1, 0.5, 1.0, 2.0, 5.0 and 10.0 mg/mL） were added into the alloxan pretreated culture medium for 1 d, 3 d, and 5 d, respectively. The survival rate was measured by MTY assay. The glucose-stimulated insulin secretion was determined by the Micro BCA protein assay kit with albumin as standard. SOD activity, MDA content, and GSH level were assayed by SOD, MDA, and GSH assay kit according to the manufacturer instructions. Results： the survival rate of cells treated with POP I increased significantly. POP I also significantly reduced oxidative damages induced by alloxan in INS-1 cells, as indicated by a decrease in MDA levels, increase in SOD activity and GSH levels. Furthermore, the sensitivity of the cells to glucose- stimulated insulin secretion was also improved in the presence of POP I in a dose-dependent manner. Conclusions： these results demonstrate that POP I can prevent alloxan-induced pancreatic β-cell damage. And the mechanism in reduced oxidative damages is strongly recommended.