Targeting Reactive Oxygen Species in Atherosclerosis via Chinese Herbal Medicines

Zhang, Leyi; Jiaqin, Huang; Zhang, Danli; Lei, Xiaojing; Ma, Yan; Cao, Yun; Chang, Jingling

doi:10.1155/2022/1852330

Cited by 6 publications

(4 citation statements)

References 125 publications

(118 reference statements)

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“…Ginsenosides, generally classified into protopanaxadiol and propanaxatriol due to the difference in C-6 chiral carbon substitution sites, are the main active components of P. ginseng used for the treatment of metabolic syndrome and CVDs ( Fan et al, 2020 ; Im, 2020 ). Most Chinese patent medicines containing ginsenosides had been applied for AS, such as Shexiang Baoxin Pill, Yixingtongmai decoction, Tongxinluo, Xin-Ji-Er-Kang, and Tiaopi Huxin recipe ( Zhang et al, 2022 ). Previous studies showed that protopanaxadiol-type ginsenoside Rd, Rb1, and Rg3 exhibited anti-atherosclerotic effects ( Xue et al, 2021 ), and ginsenoside Rb1 could regulate gut microbiota and amino acid metabolism to improve HFD-induced insulin resistance in mice ( Yang et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Ginsenoside Rc ameliorated atherosclerosis via regulating gut microbiota and fecal metabolites

Xie¹,

Zu²,

Wang³

et al. 2022

Front. Pharmacol.

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Atherosclerosis (AS) and the accompanied cardiovascular diseases (CVDs) were the leading cause of death worldwide. Recently, the association between CVDs, gut microbiota, and metabolites had aroused increasing attention. In the study, we headed our investigation into the underlying mechanism of ginsenoside Rc (GRc), an active ingredient of ginsenosides used for the treatment of CVDs, in apolipoprotein E-deficient (ApoE −/− ) mice with high-fat diet (HFD). Sevenweek-old male ApoE −/− mice were randomly divided into four groups: the normal control (NC) group, the HFD group, the GRc group (40 mg/kg/d), and the atorvastatin (Ato) group (10 mg/kg/d). Atherosclerotic injury was evaluated by aortic lesions, serum lipid levels, and inflammatory factors. The composition of gut microbiota and fecal metabolite profile were analyzed using 16S rRNA sequence and untargeted metabolomics, respectively. The results showed that GRc significantly alleviated HFD-induced aortic lesions, reduced serum levels of total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C), tumor necrosis factor-α (TNF-α), and interleukin (IL)-6 and IL-1β, and increased high-density lipoprotein cholesterol (HFD-C) level, as well as the alteration of gut microbiota composition, function, and metabolite profile. GRc also reversed HFD change of Bacteroidetes and Firmicutes at the phylum level, Muribaculaceae, Lactobacillus, Ileibacterium, Bifidobacterium, Faecalibaculum, Oscillibacter, Blautia, and Eubacterium_coprostanoligenes_group at the genus level, and 23 key metabolites involved in taurine and hypotaurine metabolism, arginine biosynthesis, ATP-binding cassette (ABC) transporters, primary bile acid biosynthesis, purine metabolism, tricarboxylic acid (TCA) cycle, and glucagon signaling pathways. Additionally, eight differential intestinal floras at the genus level were associated with 23 key differential metabolites involving atherosclerotic injury. In conclusion, our results demonstrated that GRc ameliorated atherosclerotic injury, regulated microbial and metabolomic changes in HFD-induced ApoE −/− mice, and suggested a potential correlation among gut microbiota, metabolites, and atherosclerotic injury regarding the mechanisms of GRc against AS.

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Section: Introductionmentioning

confidence: 99%

Ginsenoside Rc ameliorated atherosclerosis via regulating gut microbiota and fecal metabolites

Xie¹,

Zu²,

Wang³

et al. 2022

Front. Pharmacol.

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show abstract

“…In addition to inflammation, oxidative stress also plays an important role in the pathogenesis and progression of AS (Batty et al 2022). The vascular wall can produce endogenous ROS (Zhang et al 2022). However, excessive ROS can cause oxidative stress and damage blood vessels (Kattoor et al 2017) and transform LDL into ox-LDL, stimulating the formation of foam cells and the release of matrix metalloproteinases (MMPs) which can promote the infiltration and migration of inflammatory mediators, and then destroy the normal structure of tissues (Yu et al 2017;El Hadri et al 2021).…”

Section: Discussionmentioning

confidence: 99%

Protective effect of rubber seed oil on human endothelial cells

Zhang,

Huang,

et al. 2024

J Mol Histol

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Objective This study was conducted to characterize the antioxidant and anti-inflammatory properties of Rubber Seed Oil (RSO) against atherosclerosis (AS) through the study of the protective effects and mechanisms on human umbilical vein endothelial cells (HUVECs) injury induced by oxidized low-density lipoprotein (ox-LDL). Methods HUVECs were treated with RSO, ox-LDL, RSO + ox-LDL, respectively, followed by cell activity testing, levels of IL-1β, IL-6, IL-10, TNF-α, ROS, NO, the mRNA expression of eNOS and protein expression of MCP-1, VCAM-1, eNOS, TLR4, NF-κB p65、p-NF-κB p65. Results Compared with the ox-LDL group, cell viability, NO level and the expression of eNOS mRNA significantly increased. and the levels of pro-inflammatory factors such as IL-1β, IL-6, TNF-α, IL-10, ROS were significantly decreased, which was accompanied by decreases in TLR4 mRNA, TLR4, MCP-1, VCAM-1 protein expression, as well as the ratio of NF-κB p-p65/p65 in the group treated with 250 μg/ml ox-LDL + 50 μg/ml RSO, 250 μg/ml ox-LDL + 100 μg/ml RSO, 250 μg/ml ox-LDL + 150 μg/ml RSO. Conclusions RSO can reduce the expression of pro-inflammatory mediators, oxidative factors involved in injured vascular endothelial cells, exhibiting anti-inflammatory and antioxidant properties HUVECs exposed to ox-LDL. In addition, it may alleviate endothelial cell damage by inhibiting the TLR4/NF-κB signaling pathway.

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“…In addition to the direct role of UII, the over-production of ROS may be also involved in angiogenesis [ 37 , 38 ]. As a regulator for ROS production, upregulated NOX2 induced by UII may also impair macrophage functions and/or promote angiogenesis [ 38 , 39 ]. In such a circumstance, UII may generate a vicious circle in the lesions: the more macrophages accumulate, the more ROS is produced.…”

Section: Discussionmentioning

confidence: 99%

Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits

Wei

et al. 2023

IJMS

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Accumulated evidence shows that elevated urotensin II (UII) levels are associated with cardiovascular diseases. However, the role of UII in the initiation, progression, and regression of atherosclerosis remains to be verified. Different stages of atherosclerosis were induced in rabbits by a 0.3% high cholesterol diet (HCD) feeding, and either UII (5.4 μg/kg/h) or saline was chronically infused via osmotic mini-pumps. UII promoted atherosclerotic fatty streak formation in ovariectomized female rabbits (34% increase in gross lesion and 93% increase in microscopic lesion), and in male rabbits (39% increase in gross lesion). UII infusion significantly increased the plaque size of the carotid and subclavian arteries (69% increase over the control). In addition, UII infusion significantly enhanced the development of coronary lesions by increasing plaque size and lumen stenosis. Histopathological analysis revealed that aortic lesions in the UII group were characterized by increasing lesional macrophages, lipid deposition, and intra-plaque neovessel formation. UII infusion also significantly delayed the regression of atherosclerosis in rabbits by increasing the intra-plaque macrophage ratio. Furthermore, UII treatment led to a significant increase in NOX2 and HIF-1α/VEGF-A expression accompanied by increased reactive oxygen species levels in cultured macrophages. Tubule formation assays showed that UII exerted a pro-angiogenic effect in cultured endothelial cell lines and this effect was partly inhibited by urantide, a UII receptor antagonist. These findings suggest that UII can accelerate aortic and coronary plaque formation and enhance aortic plaque vulnerability, but delay the regression of atherosclerosis. The role of UII on angiogenesis in the lesion may be involved in complex plaque development.

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Targeting Reactive Oxygen Species in Atherosclerosis via Chinese Herbal Medicines

Cited by 6 publications

References 125 publications

Ginsenoside Rc ameliorated atherosclerosis via regulating gut microbiota and fecal metabolites

Ginsenoside Rc ameliorated atherosclerosis via regulating gut microbiota and fecal metabolites

Protective effect of rubber seed oil on human endothelial cells

Urotensin II Enhances Advanced Aortic Atherosclerosis Formation and Delays Plaque Regression in Hyperlipidemic Rabbits

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