摘要
为了探讨内皮细胞的自分泌和旁分泌对受损内皮细胞的影响 ,以及下丘脑—垂体参与后对其的作用 ,将正常内皮细胞条件培养基、联胺诱导内皮细胞的条件培养基及下丘脑垂体细胞培养基加联胺诱导内皮细胞的条件培养基分别作用正常内皮细胞和受损内皮细胞 ,并检测其脂质过氧化物丙二醛和诱导型一氧化氮合酶表达的变化。结果发现 ,联胺诱导的内皮细胞条件培养基对受损内皮细胞丙二醛代谢有明显下调作用 (P <0 .0 1) ;而下丘脑垂体细胞培养基加联胺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丙二醛代谢均有下调作用 (P<0 .0 1) ,其中对受损内皮细胞下调更明显。联胺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无明显调节作用 ,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 ;下丘脑垂体细胞培养基加联胺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诱导型一氧化氮合酶均有上调作用 (P <0 .0 5 ) ,其中对受损内皮细胞上调更明显 (P <0 .0 1)。结果提示 ,内皮细胞受到联胺脂质过氧化损伤时 ,其自分泌和旁分泌作用能下调其丙二醛的代谢和上调诱导型一氧化氮合酶的表达 。
Aim To explore whether the autocrine and paracrine secretion of the damaged endothelial cells (EC) can regulate the damaged EC and the effect of hypothalamus-pituitary neuroendocrine axis on the autocrine and paracrine secretion of the damaged EC. The changes in the metabolism of lipid peroxide (LPO) and the expression of inducible nitric oxide synthase (iNOS) were detected through the influence of conditioned media of endothelial cells (EC-CM) induced by diamide and affected by hypothalamus-pituitary cells on injured EC respectively. Methods The normal EC-CM was used in the control group. In the experimental group, the EC-CM induced by diamide and the EC-CM induced by both conditioned medium of hypothalamus-pituitary cells and diamide were prepared. The EC injured by diamide were cultured respectively with the above three EC-CM. 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 and iNOS. Results It was shown the EC-CM induced by diamide and the EC-CM induced by both conditioned medium of hypothalamus-pituitary cells and diamide had down regulative effect on the metabolism of LPO and up regulative effect on iNOS expression of injured EC. However, the medium containing hypothalamus-pituitary tissue showed more intensive anti-lipid peroxidation effect. Conclusion It is suggested that when EC was damaged by diamide, its autocrine and paracrine secretion can regulate its LPO metabolism down and regulate its iNOS expression up, which might be one of the mechanisms in EC for defending against external injury.
出处
《中国动脉硬化杂志》
CAS
CSCD
2002年第4期291-293,共3页
Chinese Journal of Arteriosclerosis
基金
江西省自然科学基金资助
关键词
动脉粥样硬化
下丘脑
血管内皮
一氧化氮
脂质过氧化作用
Atherosclerosis
Hypothalamus
Pituitary Gland
Endothelium, Vascular
Nitric Oxide
Lipid peroxidation
