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为探讨胶原的存在对细胞摄取氧化低密度脂蛋白（ｏｘ－ＬＤＬ）的影响，本研究在体外制成Ⅰ型胶原凝胶和巨噬细胞实验体系。ＬＤＬ经Ｃｕ２＋催化氧化，丙二醛（ＭＤＡ）及乙酰化修饰后，与胶原的结合能力明显增强，但４－羟基壬烯醛（ＨＮＥ）修饰的ＬＤＬ与胶原的结合能力反而不如天然ＬＤＬ。当小鼠腹腔巨噬细胞培养在胶原凝胶上时，其对ｏｘ－ＬＤＬ的摄取明显减少，这时大部分ｏｘ－ＬＤＬ为胶原凝胶所结合。如用细胞松弛素Ｄ（细胞非特异性吞噬抑制剂）处理巨噬细胞，在无胶原存在时，可见细胞对ｏｘ－ＬＤＬ的降解明显减少；而有胶原时，细胞的降解量则无明显变化，其水平与无胶原时的细胞处理组相当。上述结果提示，Ⅰ型胶原的存在可能阻止了巨噬细胞通过非特异性吞噬途径摄取ｏｘ－ＬＤＬ。
In order to investigate the effect of collagen on cellular uptake of oxidized low density lipoprotein (ox-LDL), the experimental system of type Ⅰ collagen gel and macrophage was made in vitro. LDL catalyzed by Cu2 + oxidation, malondialdehyde (MDA) and acetylation modified significantly enhanced the binding capacity of collagen, but 4-hydroxy-nonenal (HNE) modified LDL and collagen binding capacity but not as good as native LDL. When mouse peritoneal macrophages cultured on collagen gel, their uptake of ox-LDL was significantly reduced, when most of ox-LDL is bound by collagen gel. When treated with cytochalasin D (a nonspecific phagocytic inhibitor), macrophages were observed in the absence of collagen, visible degradation of ox-LDL cells was significantly reduced; collagen, the degradation of cells did not change significantly, Its level is comparable to the cell-treated group without collagen. The above results suggest that the presence of type I collagen may prevent macrophages from uptake of ox-LDL through a non-specific phagocytic pathway.