Abstract: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.

Abstract:Compared with giving native low density lipoprotein(LDL) intravenously,scavenger receptor(SR)mRNA levels in liver and spleen of the mice given mildly modified LDL(mm-LDL)intravenously increased 2. 0 times (p<0. 05)and 5.9 times(p<0. 01),respectively;and macrophage colony-stimulating factor(MCSF)mRNA levels also increased 3.2 times(p<0. 01) and 3. 0 times p<0. 01) respectively.Giving MCSF intravenously to mice increased SR mRNA levels in liver and spleen by 3. 6 times(p<0. 05) and 3. 0 times (p<0.01),respectively, and showed some dose-effect relationship.It suggests that giving mm-LDL intravenously might directly induce the expression of SR mRNA in liver and spleen,orindirectly stimulate the expression of MCSF,which in turm induces SR mRNA expression,The significance of these phenomena for local atherogenesis is discussed.