Curcumin inhibits the formation of atherosclerosis in ApoE−/− mice by suppressing cytomegalovirus activity in endothelial cells
Curcumin (Cur) is a hydrophobic polyphenol compound derived from the rhizome of the herb Curcuma longa. Cur has a wide spectrum of biological and pharmacological activities. It has been shown that human cytomegalovirus (HCMV) infection was an important risk factor for atherosclerosis (AS) and Cur ex...
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Veröffentlicht in: | Life sciences (1973) 2020-09, Vol.257, p.117658-117658, Article 117658 |
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Sprache: | eng |
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Zusammenfassung: | Curcumin (Cur) is a hydrophobic polyphenol compound derived from the rhizome of the herb Curcuma longa. Cur has a wide spectrum of biological and pharmacological activities. It has been shown that human cytomegalovirus (HCMV) infection was an important risk factor for atherosclerosis (AS) and Cur exhibited an outstanding anti-HCMV effect. However, anti-AS effects of Cur remain unclear when HCMV infected endothelial cells.
This study will investigate the anti-AS activities and mechanism of Cur,when HCMV infected in vivo and in vitro.
Cur (0.5, 1, and 2 μM) was used to explore the anti-AS activities and mechanism after HCMV infected endothelial cells in vitro. ApoE−/− mice were fed a high fat and cholesterol diet (HD) and given 4000,000 copies/mouse MCMV infection by intraperitoneal and treated with ganciclovir (5 mg/kg/d), Cur (25, 15 mg/kg/d) for 10 weeks in vivo.
As our results showed that Cur inhibited CMV replication and proliferation, reduced the intracellular ROS overproduction, decreased the release of inflammatory cytokines, down-regulated the level of HMGB1-TLRS-NF-κB signaling pathway-related proteins in vitro experiments. Cur reduced the serum levels of LDL-C, TC and TG, significantly decreased the formation of atherosclerotic plaque in the aorta, reduced the lipid deposition in liver and inflammatory damage in heart, lung and kidney in vivo experiments.
This study showed that Cur prevent AS progression by inhibiting CMV activity and CMV-induced HMGB1-TLRS-NF-κB signaling pathway.
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ISSN: | 0024-3205 1879-0631 |
DOI: | 10.1016/j.lfs.2020.117658 |