These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: DBZ blocks LPS-induced monocyte activation and foam cell formation via inhibiting nuclear factor-ĸB. Author: Xie X, Wang S, Xiao L, Zhang J, Wang J, Liu J, Shen X, He D, Zheng X, Zhai Y. Journal: Cell Physiol Biochem; 2011; 28(4):649-62. PubMed ID: 22178877. Abstract: BACKGROUND/AIMS: It has been widely accepted that chronic inflammation plays important roles in the atherogenesis. Danshensu Bingpian Zhi (DBZ) is a novel synthetic compound derived from the traditional Chinese medicine (TCM) formula Fu Fang Dan Shen (FFDS), which is effective on atherosclerosis clinically. We hypothesized that DBZ possessed the anti-atherosclerosis potentials. Here, we examined the inhibitory effects of DBZ on LPS-induced monocyte activation and foam cell formation. METHODS: The effects of DBZ were assessed on LPS-induced inflammatory factors expression in monocyte/macrophage. Activation of NF-κB and AP-1 was analyzed by luciferase reporter assay and signaling pathway of NF-κB was investigated to elucidate mechanisms underlying DBZ mediated anti-inflammatory activity. Effects of DBZ on macrophage lipid accumulation were evaluated in native LDL and LPS co-incubated macrophages. RESULTS: DBZ inhibited LPS-induced inflammatory factors expression dose dependently in monocytes. DBZ inhibited NF-κB activation strongly and AP-1 slightly. DBZ suppressed the LPS-induced degradation of IκBα, thereby decreasing the translocation of p65 to nucleus. Furthermore, DBZ suppressed LPS-activated macrophages lipid accumulation, partly due to inhibiting the expression of LPS-induced aP2 and ADRP in macrophges. CONCLUSION: These results demonstrate that DBZ has potentials on anti-atherosclerosis by suppressing monocyte activation and foam cell formation.[Abstract] [Full Text] [Related] [New Search]