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作 者:张伯科[1] 王宝琳[1] 杨霁云[1] 谌贻璞[2] 章净霞
机构地区:[1]北京医科大学第一医院儿科,100034 [2]北京医科大学第一医院内科,100034 [3]北袁医科大学生物物理教研室
出 处:《中华肾脏病杂志》1994年第4期239-240,共2页Chinese Journal of Nephrology
摘 要:硫酸类肝素蛋白多糖(HSPG)是肾小球基底膜的重要成份,参与维持肾小球毛细血管壁电荷屏障功能。体外培养的大鼠肾小球上皮细胞(GEC)合成的含硫酸根SO_2^(2-)大分子物质主要是HSPG。我们采用~3H-TdR、^(35)S-Na_2SO_4双核素标记技术,分别观察了脂多糖(LPS)、鱼精蛋白和人重组自介素-2(HrIL—2)对亚培养一代大鼠GEC增殖和细胞层^(35)SO_4^(2-)掺入量的影响。The heparan sulfate proteoglycan(HSPG) is the major part of sulfated macromolecules synthesized by the cultured rat GECs, and plays an important role in maintaining the glomerular charge—selective function. We have investigated the effects of lipopolysaccharide (LPS, 6.25ng/ml), human recombinant interleukin—2, (HrI1—2, 2. 5u/ml), and protamine sulfate(PtS, 100μg/ml) on the proliferation of rat GEC and incorporation of 35 SO into cell layers in vitro. A method of 3 H—TdR and 35 S—Na_2SO_4 dual isotope labelling technique was used. Statistical analysis was done using analysis of variance for both 3 H—TdR uptake and 35 SO incorporation, and analysis of variance only for the latter. These results show that LPS, HrIL—2 and PtS inhibited the proliferation of rat GECs. HrIL—2 also directly inhibited the incorporation of 35 SO into cell layers, but the roles of LPS and PtS, which decreased 35 SO—content, only came from their inhibition effects on cell proliferation. We suppose that the decreased production of HSPG by GECs, may contribute to the development of proteinuria.
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