牡蛎寡肽对H2O2氧化损伤L02人肝细胞的保护作用

Protective Effects of Oyster Oligopeptide against H2O2-induced Oxidative Damage in Human L02 Cells

摘要:

为了研究牡蛎寡肽对自由基清除作用及对人肝细胞L02细胞氧化损伤的保护作用，测定了牡蛎寡肽对羟自由基（·OH）的清除率，并建立过氧化氢（hydrogen peroxide，H2O2）氧化损伤人肝细胞L02的模型，研究牡蛎寡肽对氧化损伤L02细胞的存活率、活性氧（Reactive Oxygen Species，ROS）、抗氧化酶系（superoxide dismutase/SOD，glutathione/GSH）含量的影响。结果表明，牡蛎寡肽对羟自由基的IC50为0.38 mg/mL。2 mg/mL牡蛎寡肽对于L02细胞的增殖率仍为123.98%。模型组SOD和GSH水平分别降低了40%、64.87%，而ROS增加了1倍。当添加不同剂量牡蛎寡肽后，中剂量组细胞中SOD含量几乎恢复到正常组水平，GSH活性也提高了118.89%，ROS水平降到模型组的62.43%，说明牡蛎寡肽对L02细胞无毒，能降低氧化损伤的L02细胞内的ROS水平，显著提高SOD和GSH含量，对细胞起到保护作用。因此，牡蛎寡肽对H2O2致氧化损伤的人肝L02细胞具有保护作用，可能是通过清除自由基，保护细胞内抗氧化酶系活性，抑制ROS的过多积累来实现。

Abstract:

To study the scavenging capacity of free radicals and protective effect of oyster oligopeptide against hydrogen peroxide (H2O2)-induced oxidative damage in human liver L02 cells were determined. A H2O2-induced oxidative injury model was established to analyze the influence of oyster oligopeptide on the survival rate of L02 cells, level of reactive oxygen species (ROS), and contents of antioxidant enzymes (superoxide dismutase/SOD and glutathione/GSH). Results showed that IC50 of oyster oligopeptide for hydroxyl free radical was 0.38 mg/mL. The proliferation rate of L02 cells treated with oyster oligopeptide at 2 mg / mL was still 123.98%. The levels of SOD and GHS of the model group treated with 400 μM H2O2 decreased by nearly 40% and 64.87%, respectively, while the level of ROS increased by a factor of two. After the addition of oyster oligopeptide at different concentrations, the level of SOD in the middle dosage group was almost reversed to the normal level, while the activity of GSH increasing by 118.89% and the level of ROS decreasing to 62.43% of that for the model group. These results indicated that oyster oligopeptide was nontoxic to L02 cell, and could decrease the level of ROS and enhance the contents of antioxidant enzyme SOD and GSH in the oxidative stressed L02 cells, providing protective effects on cells. Therefore, oyster oligopeptide was capable of protecting human L02 cells against H2O2-induced oxidative injury, possibly through scavenging free radicals, protecting cellular antioxidant enzymes, and inhibiting the excessive accumulation of ROS.