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
Hauptverfasser: Lv, Ya-li, Jia, Yangjie, Wan, Zirui, An, Zhuo-ling, Yang, Song, Han, Fei-fei, Gong, Li-li, Xuan, Ling-ling, Ren, Lu-lu, Zhang, Wen, Liu, He, Liu, Li-hong
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container_end_page 117658
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container_title Life sciences (1973)
container_volume 257
creator Lv, Ya-li
Jia, Yangjie
Wan, Zirui
An, Zhuo-ling
Yang, Song
Han, Fei-fei
Gong, Li-li
Xuan, Ling-ling
Ren, Lu-lu
Zhang, Wen
Liu, He
Liu, Li-hong
description 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. [Display omitted]
doi_str_mv 10.1016/j.lfs.2020.117658
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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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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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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. [Display omitted]</abstract><cop>New York</cop><pub>Elsevier Inc</pub><doi>10.1016/j.lfs.2020.117658</doi><tpages>1</tpages></addata></record>
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subjects Aorta
Apolipoprotein E
Aquatic plants
Arteriosclerosis
Atherosclerosis
blood serum
Cholesterol
Curcuma longa
Curcumin
Cytokines
Cytomegalovirus
diet
Endothelial cells
Ganciclovir
Health risks
heart
High cholesterol diet
High fat diet
HMGB1 protein
Human betaherpesvirus 5
Hydrophobicity
In vitro methods and tests
In vivo methods and tests
Infection
Infections
Inflammation
Kidneys
Lipids
liver
lungs
mice
NF-κB protein
polyphenols
Rhizomes
Risk analysis
Risk factors
Serum levels
Signal transduction
Signaling
title Curcumin inhibits the formation of atherosclerosis in ApoE−/− mice by suppressing cytomegalovirus activity in endothelial cells
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