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1.
Chinese Journal of Pathophysiology ; (12)2000.
Article in Chinese | WPRIM | ID: wpr-518258

ABSTRACT

AIM: Previous studies performed with XBP-01 in vitro indicated that XBP-01 could inhibit vascular smooth muscle cells from being transformed into foam cell and could eliminate the atherosclerotic plaque in C57 BL/6J mouse. This experiment is to investigate its mechanism of eliminating plaques in vitro. METHODS: The cultured porcine artery smooth muscle cells incubated with XBP-01 of 0.1 mg/L for 24 hours after preincubated with oxidized low density lipoprotein of 15 mg/L for 72 hours in vitro. The samples were analyzed by fluorescence microscope?confocal microscope system and flow cytometry. RESULTS: Apoptosis was triggered by being incubated with oxidized low density lipoprotein and this process was accelerated additionally by being incubated with XBP-01. CONCLUSION: XBP-01 can be effective in eliminating atherosclerotic plaque by accelerating the process in which oxidized low density lipoprotein induced smooth muscle cell apoptosis

2.
Chinese Journal of Pathophysiology ; (12)1986.
Article in Chinese | WPRIM | ID: wpr-518704

ABSTRACT

AIM: These studies aimed at exploring the alteration of intracellular Ca 2+ level in the course of macrophage-derived foam cell formation as well as its mechanism.METHODS: Foam-like cell was generated by peritoneal macrophage of C57BL/6J mouse, which is susceptible to atherosclerosis, incubated in 10 mg?L -1 oxidized low density lipoprotein for 96 hours. With the technique of Ca 2+ fluorescent indicator and the assay of NADH-oxidizing coupling spectrum-alteration, the intracellular Ca 2+ level and membranous Ca 2+ -ATPase activity of the above foam-like cell were determined.RESULTS: The foam-like macrophage Ca 2+ level was 2.7 times higher than the control macrophage, and the former Ca 2+ -ATPase activity was 24% of the later.CONCLUSION: The results suggested that macrophage-derived foam cell formation was connected with slow Ca 2+ entry or release, which possibly derived from long lasting opening of membranous Ca 2+ channels at the early stage and irreversible inactivating of membranous Ca 2+ pump at the late stage.

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