Abstract
Rhizoma Polygoni Cuspidati, a Chinese herbal medicine, has been widely used in traditional Chinese medicine for a long time. Polydatin, one of the major active ingredients in Rhizoma Polygoni Cuspidati, has been recently shown to possess extensive cardiovascular pharmacological activities. In present study, we examined the effects of Polydatin on the formation of peritoneal macrophage-derived foam cells in Apolipoprotein E gene knockout mice (ApoE−/−) and explored the potential underlying mechanisms. Peritoneal macrophages were collected from ApoE−/− mice and cultured in vitro. These cells sequentially were divided into four groups: Control group, Model group, Lovastatin group, and Polydatin group. Our results demonstrated that Polydatin significantly inhibits the formation of foam cells derived from peritoneal macrophages. Further studies indicated that Polydatin regulates the metabolism of intracellular lipid and possesses anti-inflammatory effects, which may be regulated through the PPAR-γ signaling pathways.
Highlights
Complications of atherosclerosis are the leading causes of death throughout the world
To clarify the effect of Polydatin on peritoneal macrophage-derived foam cells of ApoE−/− mice, we investigated the action of Polydatin on the uptake of ox-LDL, the metabolism of intracellular lipid, the expression of inflammatory factors, and mRNA expression of PPAR-γ, ATP-binding cassette transporter A1 (ABCA1), and cluster of differentiation antigen 36 (CD36) in peritoneal macrophage
To examine the potential effects of Polydatin on macrophage cells, the mouse macrophages were incubated with ox-LDL for 48 h in the absence or presence of Polydatin and the ultrastructure was evaluated under electron microscope
Summary
Complications of atherosclerosis are the leading causes of death throughout the world. Atherosclerosis is a chronic, inflammatory disorder characterized by the deposition of excess lipids in the arterial intima [1,2,3]. Macrophage-derived foam cells play essential roles in all stages of atherosclerosis [4]. From early fatty-streak lesions to advanced plaques, macrophage-derived foam cells are integral to the development and progression of atherosclerosis. Especially cholesterol homeostasis, plays a crucial role in the formation of foam cells [5]. Macrophage foam cell formation is a prominent feature of human atherosclerotic plaques, usually considered to be correlated to uptake of and inflammatory response to oxidized low density lipoproteins (oxLDL) [6]. The limited efficacy of current treatment strategies for atherosclerosis and its complications highlights the urgent need for new therapeutic options [7]
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