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通过叔丁基脂氢过氧化物(tbooh)对巨噬细胞亚超微结构损伤的研究,探讨了活性氧在动脉粥样硬化发生中的作用。扫描电镜下可见Tbooh引起培养24h后的巨噬细胞表面微绒毛缩短,48h时部分微绒毛脱落,72h时微绒毛呈散在点状,大部分细胞膜失去微绒毛。在透射电镜下可见细胞器明显减少,脂滴增多.云芝多糖(PSK)保护组培养72h后,其胞浆仍可见线粒体、粗面内质网。可见PSK可减轻tbooh引起的巨噬细胞结构损伤、脂类堆积和细胞泡沫样变化。
The effect of reactive oxygen species (ROS) on the development of atherosclerosis was investigated by studying the ultrastructural damage of macrophages by t-butyl hydroperoxide (tbooh). Scanning electron microscopy showed that Tbooh induced shortening of microvilli on the surface of macrophages after culturing for 24 hours and shedding of some microvilli at 48h. Microvilli were scattered at 72h, and most of the cell membrane lost microvilli. Under the TEM, the organelles were obviously reduced and lipid droplets increased.After cultured for 72h, the cytoplasm of PSK protective group still showed mitochondria and rough endoplasmic reticulum. Visible PSK can reduce tbooh induced macrophage structural damage, lipid accumulation and cellular foam-like changes.