核桃粕多酚对HepG2细胞氧化损伤保护作用的研究

Walnut Meal Polyphenols Protect HepG2 Cells from Oxidative Damage

为了研究核桃粕多酚对H_(2)O_(2)诱导HepG2细胞氧化损伤的保护作用,以核桃粕为原料,采用超声辅助法在真空条件下提取多酚,HPD-100型大孔树脂纯化多酚,并对核桃粕多酚体外抗氧化活性进行测定;用CCK-8法测定不同浓度核桃粕多酚对HepG2细胞的毒性作用,以770μmol/L的H_(2)O_(2)诱导HepG2细胞建立氧化应激模型,通过测定HepG2氧化损伤细胞中MDA含量、SOD活力、GSH的含量的变化情况,研究在12.5、25、50μg/mL无毒性作用浓度下核桃粕多酚对HepG2细胞氧化损伤的保护作用。结果显示,纯化后的核桃粕多酚含量为77.53%;在同一浓度范围内,核桃粕多酚对DPPH自由基清除率与VC相比无显著差异;核桃粕多酚能使受氧化损伤的HepG2细胞内MDA含量明显减少,并且能提高受氧化损伤细胞内SOD活力以及GSH含量。综上所述,核桃粕多酚含量丰富,具有良好的体外抗氧化活性,对HepG2细胞的氧化损伤具有保护作用。

This paper aims to study the effect of walnut meal polyphenols against H_(2)O_(2)-induced oxidative damage in HepG2 cells.To be specific,the polyphenols of walnut meal were extracted by ultrasound-assisted extraction under vacuum conditions and purified by HPD-100 macroporous resin,and then the in-vitro antioxidant activity was tested.The toxicity of walnut meal polyphenols at different concentration to HepG2 cells was examined by Cell Counting Kit-8(CCK-8),and 770μmol/L H_(2)O_(2) was used to induce oxidative stress in HepG2 cells.The effect of walnut meal polyphenols at 12.5,25,and 50μg/mL(nontoxic)against oxidative damage in HepG2 cells was evaluated based on the changes of malondialdehyde(MDA)content,superoxide dismutase(SOD)activity,and glutathione(GSH)content in the cells.The results showed that the content of purified walnut meal polyphenols was 77.531%.The DPPH-scavenging rate of walnut meal polyphenols was insignificantly different from that of VC in the same concentration range.Walnut meal polyphenols significantly reduced the MDA content and increased the SOD activity and GSH content in HepG2 cells with oxidative injury.In conclusion,walnut meal was rich in polyphenols and the polyphenols had satisfactory in-vitro antioxidant activity and thus protect HepG2 cells from oxidative injury.