摘要
为了探讨受损内皮细胞的自分泌和旁分泌对受损内皮细胞本身的影响 ,本文收集正常内皮细胞条件培养基和用氧化型低密度脂蛋白 (OX-L DL )诱导内皮细胞的条件培养基分别作用于正常内皮细胞和氧化受损内皮细胞 ,检测其脂质过氧化物和一氧化氮代谢及诱导型一氧化氮合酶表达的变化。得到的结果是 :(1)正常内皮细胞的条件培养基和 OX-LDL 诱导的内皮细胞条件培养基对正常内皮细胞和受损内皮细胞脂质过氧化代谢有明显下调作用 (P<0 .0 5 ) ,但 OX-LDL 诱导的内皮细胞条件培养基的下调作用更为明显 (P<0 .0 1)。 (2 )正常内皮细胞的条件培养基和 OX-LDL 诱导的内皮细胞条件培养基对正常内皮细胞 NO的代谢表现为抑制作用 (P>0 .0 5 ) ,而对受损内皮细胞有轻微上调作用 (P>0 .0 5 )。 (3 )正常内皮细胞的条件培养基和 OX-L DL诱导的内皮细胞条件培养基对正常内皮细胞诱导型一氧化氮合酶的表达表现出抑制作用 ,而对受损内皮细胞诱导型一氧化氮合酶的表达有上调作用 (P>0 .0 5 )。本文结果提示 :正常和受到氧化损伤内皮细胞的自分泌和旁分泌作用对正常和受损内皮细胞的脂质过氧化物的代谢均有下调作用 ,对 NO的代谢和诱导型一氧化氮合酶的表达则起抑制作用 ,而对受损内皮细胞有轻微上调作用。
To explore whether the autocrine and paracrine secretion of the damaged endothelial cells (EC) can regulate the damaged EC by detecting the changes in the metabolism of lipid peroxide (LPO) and nitric oxide and the expression of inducible nitric oxide synthase (iNOS) through the influence of conditioned media of endothelial cells (EC-CM) induced by oxidized low density lipoprotein, the ordinary media was used in the control group. In the experimental group, The normal EC-CM and EC-CM induced by oxidized low density lipoprotein was prepared. The normal EC and EC injured by oxidized low density were cultured respectively with the above three media. After culturing with the three EC-CM, all EC of the experimental and control groups were cultured in serum-free medium. Then the supernatant of the above serum-free media and cultured EC were collected for detecting the content of LPO, NO and iNOS. It was shown that the normal EC-CM and the EC-CM induced by oxidized low density lipoprotein had down regulative effect on the metabolism of LPO and up regulative effect on the metabolism of NO and iNOS expression of injured EC. It is suggested that when EC was damaged by oxidized low density, its autocrine and paracrine secretion can down regulate its LPO metabolism and up regulate the metabolism of NO and its iNOS expression, which might be one of the mechanisms in EC for defending against external injury.
出处
《神经解剖学杂志》
CAS
CSCD
北大核心
2003年第3期307-310,共4页
Chinese Journal of Neuroanatomy
