曲格列酮和罗格列酮可抑制低密度脂蛋白诱导的血管平滑肌细胞生长。
Troglitazone and rosiglitazone inhibit the low density lipoprotein-induced vascular smooth muscle cell growth.
作者信息
Gouni-Berthold I, Berthold H K, Weber A A, Seul C, Vetter H, Sachinidis A
机构信息
Medizinische Universitäts-Poliklinik, Bonn, Germany.
出版信息
Exp Clin Endocrinol Diabetes. 2001;109(4):203-9. doi: 10.1055/s-2001-15107.
Troglitazone (TRO) and rosiglitazone (RSG) belong to the thiazolidinedione class (insulin-sensitizing agents) and exert many of their metabolic effects as peroxisome proliferator-activated receptor gamma (PPARgamma) ligands. In the present study we examined the effects of TRO and RSG on LDL-induced VSMC growth. Pretreatment of VSMC with 1 microM TRO or 0.1 microM RSG completely blocked the LDL-induced cell proliferation as measured by [3H]thymidine incorporation into DNA and by determination of the cell number. We then examined with Western blotting whether these growth suppressing effects are mediated through the mitogen-activated protein kinase (MAPK) pathway, a common signaling pathway activated by growth factors. TRO and RSG had no effect on the LDL-induced stimulation of the MAP kinases ERK1/2, p38 and SAP/JNK. We conclude that thiazolidinediones are potent inhibitors of LDL-induced VSMC growth acting downstream of the cytoplasmic activation of MAPK.
曲格列酮（TRO）和罗格列酮（RSG）属于噻唑烷二酮类（胰岛素增敏剂），作为过氧化物酶体增殖物激活受体γ（PPARγ）配体发挥多种代谢作用。在本研究中，我们检测了TRO和RSG对低密度脂蛋白（LDL）诱导的血管平滑肌细胞（VSMC）生长的影响。用1微摩尔/升TRO或0.1微摩尔/升RSG预处理VSMC，通过[3H]胸腺嘧啶核苷掺入DNA以及测定细胞数量来衡量，结果显示其完全阻断了LDL诱导的细胞增殖。然后，我们用蛋白质印迹法检测这些生长抑制作用是否通过丝裂原活化蛋白激酶（MAPK）途径介导，该途径是由生长因子激活的常见信号通路。TRO和RSG对LDL诱导的MAP激酶ERK1/2、p38和SAP/JNK的激活没有影响。我们得出结论，噻唑烷二酮类是LDL诱导的VSMC生长的有效抑制剂，作用于MAPK胞质激活的下游。
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