Hyperoside suppresses tumor necrosis factor α-mediated vascular inflammatory responses by downregulating mitogen-activated protein kinases and nuclear factor-κB signaling

Jang, Seon‐A; Park, Dae Won; Sohn, Eun Hwa; Lee, Sung Ryul; Kang, Se Chan

doi:10.1016/j.cbi.2018.08.013

Cited by 25 publications

(18 citation statements)

References 48 publications

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“…Thus, the THP-1 cells adhesion assay was performed. In the presence of erastin, the adhesion of THP-1 cells to HASMCs significantly increased, although it was less effective than TNFα, which has been verified to stimulate vascular inflammatory responses through stimulating the expression of vascular cell adhesion molecule-1 (VCAM-1) in VSMCs ( 37 ). Co-administration of erastin and TNFα showed a significantly stronger effect than treatment with TNFα individually ( Figure 9 ).…”

Section: Resultsmentioning

confidence: 99%

Identification of HMOX1 as a Critical Ferroptosis-Related Gene in Atherosclerosis

Wang

et al. 2022

Front. Cardiovasc. Med.

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Ferroptosis is a novel form of programmed iron-dependent cell death. The ferroptosis-related genes (FRGs) have been recognized as biomarkers for cancers. Increasing evidence has indicated that ferroptosis is involved in the process of atherosclerosis. However, the potential FRGs used for the diagnosis, prognosis and therapy for atherosclerosis are still unclear. We aimed to identify the ferroptosis-related differentially expressed genes (DEGs) of atherosclerosis. We downloaded the mRNA-sequencing data of patients with atherosclerosis from the Gene Expression Omnibus (GEO) database. HMOX1 was identified as an essential ferroptosis-related DEG by bioinformatic analysis of the GSE28829 and GSE43292 datasets. The pro-ferroptotic effect of HMOX1 was validated through cell experiments. Then we conducted a single-gene analysis of HMOX1 and found that high-expression of HMOX1 in atherosclerotic plaques was accompanied by matrix metalloproteinases (MMPs) producing and M0 macrophages infiltration. Taken together, our present study suggested HMOX1 as a potential diagnostic biomarker for atherosclerosis and provided more evidence about the vital role of ferroptosis in atherosclerosis progression.

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Section: Resultsmentioning

confidence: 99%

Identification of HMOX1 as a Critical Ferroptosis-Related Gene in Atherosclerosis

Wang

et al. 2022

Front. Cardiovasc. Med.

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“…Therefore, we speculated that hyperoside-induced apoptosis might be related to the NF-κB signaling pathway. Hyperoside reduced neurotoxicity of microglial cells by inhibiting the phosphorylation of p38 and p65 proteins [26], and it could inhibit tumor necrosis factor-alpha-mediated vascular inflammation [44]. We evaluated proteins of NF-κB pathway in MCF-7 cells and 4T1 cells.…”

Section: Discussionmentioning

confidence: 99%

Hyperoside Induces Breast Cancer Cells Apoptosis via ROS-Mediated NF-κB Signaling Pathway

Qiu

Zhang

Zhu

et al. 2019

IJMS

104

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Hyperoside (quercetin 3-o-β-d-galactopyranoside) is one of the flavonoid glycosides with anti-inflammatory, antidepressant, and anti-cancer effects. But it remains unknown whether it had effects on breast cancer. Here, different concentrations of hyperoside were used to explore its therapeutic potential in both breast cancer cells and subcutaneous homotransplant mouse model. CCK-8 and wound healing assays showed that the viability and migration capability of Michigan Cancer Foundation-7 (MCF-7) and 4T1 cells were inhibited by hyperoside, while the apoptosis of cells were increased. Real-time quantitative PCR (qRT-PCR) and western blot analysis were used to detect mRNA and the protein level, respectively, which showed decreased levels of B cell lymphoma-2 (Bcl-2) and X-linked inhibitor of apoptosis (XIAP), and increased levels of Bax and cleaved caspase-3. After exploration of the potential mechanism, we found that reactive oxygen species (ROS) production was reduced by the administration of hyperoside, which subsequently inhibited the activation of NF-κB signaling pathway. Tumor volume was significantly decreased in subcutaneous homotransplant mouse model in hyperoside-treated group, which was consistent with our study in vitro. These results indicated that hyperoside acted as an anticancer drug through ROS-related apoptosis and its mechanism included activation of the Bax–caspase-3 axis and the inhibition of the NF-κB signaling pathway.

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“…The S100A8/A9 heterodimer is also known as a ligand of the receptor for advanced glycation end products (RAGE) and is associated with atherogenesis (25). It is likely that these inflammatory cytokines and S100 proteins should trigger the production of adhesion molecules, such as E-selectin, intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1, which enhance the attachment of leukocytes to blood vessels (26)(27)(28).…”

Section: Discussionmentioning

confidence: 99%

Undernutrition in Pregnant Rats Induces Glucose Intolerance with Enhanced Expression of Inflammation-Related Genes in Peripheral Leukocytes of the Offspring

Jin

Honma

Mochizuki

et al. 2019

J Nutr Sci Vitaminol

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Impaired glucose tolerance (IGT) induces chronic inflammation and subsequent development of complications triggered by arteriosclerosis. Moreover, undernutrition in pregnant rodents can induce IGT in their offspring. Here, we assessed whether undernutrition in pregnant rats would induce chronic inflammation in their offspring by measuring the expression levels of inflammation-related genes in peripheral blood leukocytes. Pregnant Wistar rats were divided into two groups: the control group received an American Institute of Nutrition Rodent diet (AIN-93G) ad libitum, and the undernutrition group had their diet restricted by 50% (w/w) compared with the control group from day 10 of pregnancy until birth of the offspring. Subsequently, mothers and pups were allowed to access the AIN-93G diet freely. At day 35 after birth, male pups were fasted for 4 h and subsequently orally administered with glucose solution (2 g/kg body weight). Blood glucose area under the curve (AUC) after glucose loading was significantly greater in the undernutrition group than the control group. The mRNA levels for inflammatory cytokines were increased by glucose loading especially in the undernutrition group. Expressions of genes encoding S100A9 and cell adhesion molecule CD11b were increased by glucose loading in the undernutrition group. Thus, undernutrition of pregnant rats during mid to late gestation induced the expression of inflammation-related genes in peripheral blood leukocytes of their offspring, with the development of IGT and impaired insulin secretion.

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Hyperoside suppresses tumor necrosis factor α-mediated vascular inflammatory responses by downregulating mitogen-activated protein kinases and nuclear factor-κB signaling

Cited by 25 publications

References 48 publications

Identification of HMOX1 as a Critical Ferroptosis-Related Gene in Atherosclerosis

Identification of HMOX1 as a Critical Ferroptosis-Related Gene in Atherosclerosis

Hyperoside Induces Breast Cancer Cells Apoptosis via ROS-Mediated NF-κB Signaling Pathway

Undernutrition in Pregnant Rats Induces Glucose Intolerance with Enhanced Expression of Inflammation-Related Genes in Peripheral Leukocytes of the Offspring

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