Promoting reverse cholesterol transport contributes to the amelioration of atherosclerosis by paeoniflorin.

Reverse cholesterol transport (RCT) offers a practical approach to mitigating atherosclerosis. Paeoniflorin, a monoterpenoid glycoside found in plants of the Paeoniaceae family, has shown various effects on cardiovascular and liver diseases. Nevertheless, its impact on atherosclerosis in vivo remains poorly understood.

MDM2-Mediated Ubiquitination of RXRβ Contributes to Mitochondrial Damage and Related Inflammation in Atherosclerosis.

A novel function of retinoid X receptor beta (RXRβ) in endothelial cells has been reported by us during the formation of atherosclerosis. Here, we extended the study to explore the cellular mechanisms of RXRβ protein stability regulation. In this study, we discovered that murine double minute-2 (MDM2) acts as an E3 ubiquitin ligase to target RXRβ for degradation.

Activating PGC-1α-mediated signaling cascades in the aorta contributes to the amelioration of vascular senescence and atherosclerosis by 2,3,4',5-tetrahydroxystilbene-2-O-β-d-glycoside.

Background: 2,3,4',5-tetrahydroxystilbene-2-O-β-d-glycoside (TSG), the main active polyphenolic component of Polygonum multiflorum, possesses many pharmacological activities. Its anti-aging effect influences a variety of tissues with diverse mechanisms. However, the effectiveness and exact mechanisms of TSG against vascular senescence in atherosclerosis remain unclear.

Overexpression of retinoid X receptor beta provides protection against oxidized low-density lipoprotein-induced inflammation via regulating PGC1α-dependent mitochondrial homeostasis in endothelial cells.

Retinoid X receptor beta (RXRβ) has been poorly studied in atherosclerosis. The aim of the present study is to explore the function of RXRβ in oxidized low density lipoprotein (ox-LDL)-induced inflammation in endothelial cells and the underlying mechanism. The protein expression of RXRβ in the aorta of atherosclerotic mice was detected.

Naringenin alleviates nonalcoholic steatohepatitis in middle-aged Apoemice: role of SIRT1.

Background: Naringenin is naturally isolated from citrus fruits possessing many pharmacological activities. However, little is known about the effect of naringenin on nonalcoholic steatohepatitis (NASH) in the model of metabolic syndrome.

Purpose: The present study is aimed to investigate the effect of naringenin on NASH in 12-mo-old male ApoE mice and its possible underlying mechanism.

MDM2 contributes to oxidized low-density lipoprotein-induced inflammation through modulation of mitochondrial damage in endothelial cells.

Background And Aims: Murine double minute-2 (MDM2) has been poorly studied in cardiovascular diseases. The aim of the present study was to determine the biological role of MDM2 in inflammation activation and mitochondrial damage in human aortic endothelial cells (HAECs) stimulated with oxidized low-density lipoprotein (ox-LDL).

Methods: The expression of MDM2 in the aortas of atherosclerotic mice was determined.

Modulation of SIRT1-mediated signaling cascades in the liver contributes to the amelioration of nonalcoholic steatohepatitis in high fat fed middle-aged LDL receptor knockout mice by dihydromyricetin.

Dihydromyricetin (DMY) is the most abundant flavonoid in Ampelopsis grossedentata possessing many pharmacological activities. But less is known about its protective effect against nonalcoholic steatohepatitis (NASH) in the context of metabolic syndrome. The present study is aimed to evaluate the pharmacological effects of DMY on NASH induced by feeding a high fat diet to 12-mo-old male LDLr mice for 12 weeks and its molecular mode of action.

Polydatin attenuates atherosclerosis in apolipoprotein E-deficient mice: Role of reverse cholesterol transport.

Background: Polydatin has been recently shown to possess extensive cardiovascular pharmacological activities. However, its protective effect against atherosclerosis in vivo remains poorly understood. The aim of the present study was to evaluate the potential effects of polydatin on high fat diet (HFD)-induced atherosclerosis using ApoE mice, and explore the underlying mechanisms involved, especially focusing on reverse cholesterol transport (RCT) regulation.

2, 3, 4', 5-tetrahydroxystilbene-2-0-β-d Glycoside Attenuates Age- and Diet-Associated Non-Alcoholic Steatohepatitis and Atherosclerosis in LDL Receptor Knockout Mice and Its Possible Mechanisms.

The compound, 2,3,5,4'-tetrahydroxystilbene-2-O-β-d-glucoside (TSG), a primary bioactive polyphenolic component of exerts numerous pharmacological activities. However, its protective effect against non-alcoholic steatohepatitis (NASH), in the context of metabolic syndrome, remains poorly understood. The aim of the present study is to evaluate the effects of TSG treatment on middle-aged (12-mo-old) male LDLr mice, which were fed a high fat diet for 12 weeks to induce metabolic syndrome and NASH.

Salusin-α attenuates hepatic steatosis and atherosclerosis in high fat diet-fed low density lipoprotein receptor deficient mice.

Salusin-α is an endogenous bioactive peptide and likely to prevent atherosclerosis. But its protective effect against atherosclerosis in vivo remains poorly understood. The aim of the present study was to determine the potential effects of salusin-α on atherosclerosis and its associated metabolic disorders in high fat diet (HFD)-fed low density lipoprotein receptor deficient (LDLr) mice, and also explore the possible underlying mechanisms involved.

Dihydromyricetin ameliorates foam cell formation via LXRα-ABCA1/ABCG1-dependent cholesterol efflux in macrophages.

As the most abundant flavonoid in Ampelopsis grossedentata, the protective effects of dihydromyricetin on atherosclerosis have been well established, yet the detailed mechanisms are not fully understood. The aim of the present study was to examine the effect of dihydromyricetin on lipid accumulation and the underlying molecular mechanisms in macrophages and ApoE mice. Incubation with dihydromyricetin significantly attenuated oxidized low-density lipoprotein (ox-LDL)-mediated cholesterol and lipid accumulation in THP-1-derived macrophages, which was due to increased cholesterol efflux.

2,3,4',5-tetrahydroxystilbene-2-O-β-d-glycoside attenuates atherosclerosis in apolipoprotein E-deficient mice: role of reverse cholesterol transport.

The aim of this study was to evaluate the potential effects of 2,3,4',5-tetrahydroxystilbene-2-O-β-d-glucoside (TSG) on the development of atherosclerotic plaque in ApoE mice, and explore the mechanisms involved. Our data showed that after 8 weeks of treatment, TSG ameliorated serum levels of total cholesterol, triglyceride, and low density lipoprotein cholesterol, and increased serum levels of high density lipoprotein cholesterol in ApoE mice. TSG suppressed hepatic steatosis, the formation of atherosclerotic lesions, and the formation of macrophage foam cells in ApoE mice.

Dihydromyricetin ameliorates atherosclerosis in LDL receptor deficient mice.

Background And Aims: Dihydromyricetin, the most abundant flavonoid in Ampelopsis grossedentata, exerts numerous pharmacological activities, including anti-inflammatory, antioxidant, hepatoprotective, and lipid regulatory activities; however, its protective effect against atherosclerosis remains poorly understood. The aim of the present study was to evaluate the effects of dihydromyricetin on high fat diet (HFD)-induced atherosclerosis using LDL receptor deficient (LDLr) mice.

Methods: Blood samples were collected for determination of serum lipid profiles, oxidized LDL (ox-LDL) and pro-inflammatory cytokines.

PPAR-γ is involved in the protective effect of 2,3,4',5-tetrahydroxystilbene-2-O-beta-D-glucoside against cardiac fibrosis in pressure-overloaded rats.

2, 3, 4', 5-tetrahydroxystilbene-2-0-β-D glucoside (TSG) could inhibit cardiac remodeling in response to pressure overload. Peroxisome proliferator-activated receptor gamma (PPAR-γ) has been recognized as a potent, endogenous antifibrotic factor and maintaining a proper expression level in myocardium is necessary for assuring that structure and function of heart adapt to pressure overload stress. The aim of the present study was to investigate whether PPAR-γ is involved in the beneficial effect of TSG on pressure overload-induced cardiac fibrosis.

Economic evaluation of 5-HT3 receptor antagonists in combination with dexamethasone for the prevention of 'overall' nausea and vomiting following highly emetogenic chemotherapy in Chinese adult patients.

Background Two pivotal Phase III trials compared the efficacy of palonosetron, ondansetron and granisetron, combined with dexamethasone, for the prevention of nausea and vomiting following highly emetogenic chemotherapy. However, an economic evaluation of these three regimens in the real-world setting of Chinese adult patients has not been determined. Objectives To estimate, from the perspective of the Chinese healthcare system, which of these frequently used strategies consisting of 0.

Effect of Salusin-β on Peroxisome Proliferator-Activated Receptor Gamma Gene Expression in Vascular Smooth Muscle Cells and its Possible Mechanism.

Background/aims: salusin-β is considered to be a potential pro-atherosclerotic factor. Regulation and function of vascular smooth muscle cells (VSMCs) are important in the progression of atherosclerosis. Peroxisome proliferator-activated receptor gamma (PPARγ) exerts a vascular protective role beyond its metabolic effects.

Salusin-β induces smooth muscle cell proliferation by regulating cyclins D1 and E expression through MAPKs signaling pathways.

Despite the clear mitogenic effect of salusin-β on vascular smooth muscle cells (VSMCs), which contributes to its proatherosclerotic effects, additional studies are needed to explore its underlying mechanisms. The aim of this study was to investigate the mechanism of salusin-β's effects on VSMCs cell cycle regulation and the possible signal pathways. Salusin-β accelerated the G1/S phase transition in VSMCs and increased the expression levels of cyclins D1 and E.

Inhibitory effects of 2,3,4',5-tetrahydroxystilbene-2-O-β-D-glucoside on angiotensin II-induced proliferation of vascular smooth muscle cells.

Objective: To investigate the effect of 2,3,4',5-tetrahydroxystilbene-2-O-β-D-glucoside (TSG), an active component extracted from the root of Polygonum multiflorum, on angiotensin II (Ang II)-induced proliferation of cultured rat vascular smooth muscle cells (VSMCs) and to identify the potential mechanism.

Methods: Cell proliferation and cell cycle were determined by cell counting, 5-bromo-2'-deoxyuridine incorporation assay, proliferating cell nuclear antigen protein expression and flow cytometry. Levels of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2), mitogenic extracellular kinase 1/2 (MEK1/2) and Src in VSMCs were measured by Western blot.

The effect of 2,3,4',5-tetrahydroxystilbene-2-O-β-D-glucoside on pressure overload-induced cardiac remodeling in rats and its possible mechanism.

The aim of the present study was to investigate the effects of 2,3,4',5-tetrahydroxystilbene-2-O-beta-D-glucoside, an active component extracted from Polygonum multiflorum, on pressure overload-induced cardiac remodeling in rats. A rat model with cardiac remodeling was induced by abdominal aortic banding. 2,3,4',5-Tetrahydroxystilbene-2-O-beta-D-glucoside (30, 60, 120 mg/kg/day) was administered 3 days after abdominal aortic banding and continued for 30 days.

Role of mitochondrial permeability transition in human hepatocellular carcinoma Hep-G2 cell death induced by rhein.

Rhein, a compound found as a glucoside in the root of rhubarb, is currently a subject of interest for its antitumor properties. The apoptosis of tumor cell lines induced by rhein was observed, and the involvement of mitochondria was established; however, the role of mitochondrial permeability transition (MPT) remains unknown. Here we report that MPT plays an important role in the apoptosis of human hepatocellular carcinoma Hep-G2 cells induced by rhein.

The effect of 2,3,4',5-tetrahydroxystilbene-2-0-β-D glucoside on neointima formation in a rat artery balloon injury model and its possible mechanisms.

2,3,4',5-tetrahydroxystilbene-2-0-β-D glucoside (TSG) has been recognized to suppress the proliferation of vascular smooth muscle cells (VSMCs). The aim of the present study was to determine whether TSG inhibits neointimal hyperplasia in a rat carotid arterial balloon injury model. Balloon injury was induced in the left common carotid artery of rats.

2,3,4',5-tetrahydroxystilbene-2-O-β-D-glucoside inhibits proliferation of vascular smooth muscle cells: involvement of NO/cGMP/PKG pathway.

The proliferation of vascular smooth muscle cells (VSMCs) induced by injury to the intima of arteries is an important etiologic factor in vascular proliferative disorders such as atherosclerosis and restenosis. 2,3,4',5-Tetrahydroxystilbene-2-O-β-D-glucoside (TSG), an active component extracted from Polygonum multiflorum, has been found to have an antiatherosclerotic effect. The aim of this study was to investigate the effects of TSG on platelet derived growth factor (PDGF)-BB induced VSMCs proliferation and to explore the possible mechanisms of such effects.

2,3,4',5-Tetrahydroxystilbene-2-O-β-d-glucoside inhibits platelet-derived growth factor-induced proliferation of vascular smooth muscle cells by regulating the cell cycle.

1. 2,3,4',5-Tetrahydroxystilbene-2-O-β-d-glucoside (TSG) has been shown to have an anti-atherosclerotic effect. Vascular smooth muscle cell (VSMC) proliferation contributes to the pathobiology of atherosclerosis.

Effects of 2,3,4',5-tetrahydroxystilbene 2-O-beta-D-glucoside on vascular endothelial dysfunction in atherogenic-diet rats.

2,3,4',5-Tetrahydroxystilbene 2- O-beta- D-glucoside (TSG), an active component extracted from Polygonum multiflorum, has been found to have an anti-atherosclerotic effect. The aim of this study was to investigate whether the TSG could prevent the development of atherosclerosis through influencing endothelial function in atherogenic-diet rats and to explore the possible mechanisms. Vascular endothelial dysfunction was assessed using isolated aortic ring preparation, transmission electron microscopy of the aorta, and levels of nitrate/nitrite (NOx) in serum and aorta.

[The expression of matrix metalloproteinase-2,9 on atherosclerosis in experimental rats by treatment of 2,3,4',5-tetrahydroxystilbene -2-0-beta-D glucoside].

Aim: To observe the changes of MMP-2, 9 level on atherosclerosis in experimental rats by treatment of 2,3,4',5-tetrahydroxystilbene-2-0-beta-D glucoside (TSG) and to investigate the mechanism of TSG in stabilizing plaque and anti-atherosclerosis.

Methods: The atherosclerosis model of rat was made by feeding high grease food and injecting VitD3. Sixty male SD rats were randomly divided into six groups: control, Simvastatin, model and TSG 120 mg x kg(-1) x d(-1), TSG 60 mg x kg(-1) x d(-1) and TSG 30 mg x kg(-1) x d(-1).