沥水调脂胶囊对轻度修饰低密度脂蛋白诱导血管平滑肌细胞丝裂原活化蛋白激酶信号转导的影响

轻度修饰低密度脂蛋白 ;　血管平滑肌细胞摘　要 ]　为了探讨健脾祛痰化瘀方———沥水调脂胶囊对轻度修饰低密度脂蛋白诱导的血管平滑肌细胞丝裂原活化蛋白激酶信号转导的影响 ,采用血清药理学通法制备含药血清 ,以甲醇除蛋白预处理 ;以Cu2 + 氧化制备轻度修饰低密度脂蛋白 ;用磷酸化抗体以WesternBlot方法分析c junN端激酶 1、细胞外信号调节激酶 1和 2的磷酸化。结果发现 ,2 0 %含药血清可明显降低 0 .5h和 1h轻度修饰低密度脂蛋白诱导的c junN端激酶 1磷酸化 (P <0 .0 5 ) ,而对细胞外信号调节激酶 1和 2无明显影响。结果提示 ,降低c junN端激酶 应激活化蛋白激酶信号可能是沥水调脂胶囊抑制血管平滑肌细胞增殖的机制之一。

Effect of Serum-Containing of Protein-Removed Li Shui Tiao Zhi Capsule on Mitogen-Activated Protein Kinases Signal of Vascular Smooth Muscle Cells Induced by Mildly Modified Low Density Lipoprotein

Aim To explore the effect of Li Shui Tiao Zhi capsule (LSTZ) on mitogen-activated protein kinases signal of vascular smooth muscle cells induced by mildly oxidized low density lipoprotein. Methods Serum-containing LSTZ was produced by general serum pharmacology assay method and protein was removed by methanol. LDL was oxidized by incubation with Cu 2+. c-Jun N-terminal kinase (JNK1), extracellular signal regulated kinase (ERK1/2) phosphorylation was examined by Western Blot assay. Results 20% serum-containing LSTZ significantly reduced the phosphorylated JNK1 level, but ERK1 and ERK2 phosphorylation level after mm-LDL-stimulation was not altered significantly. Conclusions The preferential reduction of the activation of the JNK/SAPK signal transduction pathway might be one of the mechanisms for inhibition of VSMC proliferation caused by LSTZ.