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LU Ci-yong, LING Wen-hua, MA Jing, . Study on signal pathway on function changing of macrophages induced by oxidized low density lipoprotein[J]. Chinese Journal of Public Health, 2003, 19(10): 1171-1173.
Citation: LU Ci-yong, LING Wen-hua, MA Jing, . Study on signal pathway on function changing of macrophages induced by oxidized low density lipoprotein[J]. Chinese Journal of Public Health, 2003, 19(10): 1171-1173.

Study on signal pathway on function changing of macrophages induced by oxidized low density lipoprotein

  •   Objective   To study the effects of oxidized low density lipoprotein on proliferation, apoptosis and necrosis of macrophages via the possible mechanism of signal transduction unrelated to scavenger receptor pathway.The role of SAPK (Stress-activated protein kinase) signal pathway were studied.
      Methods   Two-factorial experiment was designed to explore the influence of four dosage levels of Ox-LDL (0, 50, 100, 200 mg/L) at three different stages of exposure (24, 48 and 72 hr) on proliferation apoptosis and necrosis of macro phage cells of SRA (scavenger receptor A) knockout mice. Activity of SAP K in the macrophage cells of SRA knockout mice was observed with different exposure level of Ox-LDL at different times.
      Results   The apoptosis and necrosis of macrophages of SRA knockout mice induced by Ox-LDL was associated with both the exposure level and time (P < 0.01); Ox-LDL could induced the proliferation of the macrophages of SRA knockout mice, which was significantly associated with the dosage and time (P < 0.01). The activities of SAPK were changed at different dose of Ox-LDL.
      Conclusion   Proliferation was the main response to Ox-LDL, and apoptosis and necrosis were also observed for higher exposure of Ox-LDL in macrophages of SRA knockout mice. This proliferation and apoptosis induced by Ox-L DL might be partly mediated by SAPK signal pathways, which implicated that other ways might play the role in the Ox-LDL induced proliferation and apoptosis of macrophage with scavenger receptor deficiency.
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