为了比较维生素C-磷脂复合体（VitC-PC）和VitC体外抑制小鼠腹腔巨噬细胞氧化应激的活性，本研究提取小鼠腹腔巨噬细胞，在体外培养，用沙门氏菌脂多糖（LPS）诱导氧化应激，分别用不同浓度VitC和VitC-PC进行处理，测定培养液一氧化氮（NO）、乳酸脱氢酶（LDH）、丙二醛（MDA）和细胞内诱导性NO合成酶（iNOS），以评价细胞炎性反应、细胞膜完整性和脂质过氧化程度。同时静息态腹腔巨噬细胞与不同浓度的VitC或VitC-PC共孵育，测定细胞内VitC浓度，以评价细胞摄取VitC或VitC-PC的效率。结果发现，在高浓度添加VitC时，巨噬细胞摄取VitC-PC的效率高于VitC（P<0.05），VitC-PC抑制LPS诱导巨噬细胞释放NO、发生脂质过氧化（产生MDA）和细胞膜损伤（LDH泄露）的效率显著高于VitC（P<0.05）。因此，本研究证明VitC-PC比VitC更易进入细胞内部发挥抗氧化作用。

This study makes a comparative analysis of the in vitro anti-oxidative effect of vitamin C(VitC) and VitC phosphate complex (VitC-PC). Mice peritoneal macrophages were prepared and incubated in vitro. Lipopolysaccharide (LPS) of Salmonella was used to induce the oxidative stress. The cells were treated by VitC and VitC-PC of different concentrations, respectively. Extracellular nitric oxide (NO), lactic dehydrogenase (LDH) and malonaldehyde (MDA) and intraocular inducible nitric oxide synthetase (iNOS) were determined to characterize the extent of inflammatory response, the membrane integrity and the lipid peroxidation, respectively. Untreated macrophages were also incubated with VitC or VitC-PC of different concentrations, and the intraocular VitC was measured to estimate the incorporation efficiency of VitC. The results show that the macrophage uptake of VitC-PC is more significant than that of VitC in a high concentration (P<0.05). VitC-PC would inhibit LPS induced macrophage release of NO, and the lipid peroxidation occurs (to generate MDA) and the cell membrane damages (to release LDH), which is more significant than VitC (P<0.05). It is concluded that it is easier for VitC-PC than for VitC to enter into cells and to prevent the damage of high molecules by over production of free radicals.