Quince extract resists atherosclerosis in rats by down-regulating the EGFR/PI3K/Akt/GSK-3β pathway

Abulizi, Abulaiti; Simayi, Jimilihan; Nuermaimaiti, Maimaitiming; Han, Mengyuan; Hailati, Sendaer; Talihati, Ziruo; Maihemuti, Nulibiya; Nuer, Muhadaisi; Khan, Nawaz; Abudurousuli, Kayisaier; Dilimulati, Dilihuma; Nueraihemaiti, Nuerbiye; Moore, Nicholas; Wumaier, Ainiwaer; Zhou, Wenting

doi:10.1016/j.biopha.2023.114330

Cited by 16 publications

(7 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In this study, R-hirudin decreased ET-1 and TXB2 levels, and increased 6-K-PGF1 α and NO levels. This was similar to the findings of Abulizi et al (2023) , who identified increased serum NO and 6-K-PGF1 α levels, decreased ET-1 and TXB2 levels in rats with atherosclerosis, resulting in anti-thrombotic outcomes. Therefore, we made the hypothesis that R-hirudin attenuated oxidative stress and inflammatory response, suppressed platelet aggregation, and promoted restoration of vascular endothelial function in APE rats, which in turn exerted anti-thrombotic effects and protective effects on lung tissues.…”

Section: Discussionsupporting

confidence: 90%

Recombinant hirudin attenuates pulmonary hypertension and thrombosis in acute pulmonary embolism rat model

Wei,

Zou,

Dong

et al. 2024

PeerJ

View full text Add to dashboard Cite

Background Acute pulmonary embolism (APE) is classified as a subset of diseases that are characterized by lung obstruction due to various types of emboli. Current clinical APE treatment using anticoagulants is frequently accompanied by high risk of bleeding complications. Recombinant hirudin (R-hirudin) has been found to have antithrombotic properties. However, the specific impact of R-hirudin on APE remains unknown. Methods Sprague-Dawley (SD) rats were randomly assigned to five groups, with thrombi injections to establish APE models. Control and APE group rats were subcutaneously injected with equal amounts of dimethyl sulfoxide (DMSO). The APE+R-hirudin low-dose, middle-dose, and high-dose groups received subcutaneous injections of hirudin at doses of 0.25 mg/kg, 0.5 mg/kg, and 1.0 mg/kg, respectively. Each group was subdivided into time points of 2 h, 6 h, 1 d, and 4 d, with five animals per point. Subsequently, all rats were euthanized, and serum and lung tissues were collected. Following the assessment of right ventricular pressure (RVP) and mean pulmonary artery pressure (mPAP), blood gas analysis, enzyme-linked immunosorbnent assay (ELISA), pulmonary artery vascular testing, hematoxylin-eosin (HE) staining, Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining, immunohistochemistry, and Western blot experiments were conducted. Results R-hirudin treatment caused a significant reduction of mPAP, RVP, and Malondialdehyde (MDA) content, as well as H2O2 and myeloperoxidase (MPO) activity, while increasing pressure of oxygen (PaO2) and Superoxide Dismutase (SOD) activity. R-hirudin also decreased wall area ratio and wall thickness to diameter ratio in APE rat pulmonary arteries. Serum levels of endothelin-1 (ET-1) and thromboxaneB2 (TXB2) decreased, while prostaglandin (6-K-PGF1α) and NO levels increased. Moreover, R-hirudin ameliorated histopathological injuries and reduced apoptotic cells and Matrix metalloproteinase-9 (MMP9), vascular cell adhesion molecule-1 (VCAM-1), p-Extracellular signal-regulated kinase (ERK)1/2/ERK1/2, and p-P65/P65 expression in lung tissues. Conclusion R-hirudin attenuated pulmonary hypertension and thrombosis in APE rats, suggesting its potential as a novel treatment strategy for APE.

show abstract

Section: Discussionsupporting

confidence: 90%

Recombinant hirudin attenuates pulmonary hypertension and thrombosis in acute pulmonary embolism rat model

Wei,

Zou,

Dong

et al. 2024

PeerJ

View full text Add to dashboard Cite

show abstract

“…They are thought to help Uyghurs maintain longer survival rates and lower blood pressure compared to other Central Asian populations. This type of C. oblonga activity has been experimentally supported by research by Albiz et al [169], Zhou et al [170][171][172], and Abulizi et al [173]. In the studies by Abliz et al [169], ethanolic leaf extract reduced total cholesterol, triglycerides, LDL-cholesterol and MDA, inhibited the activity of aminotransferase (ALT), aspartate aminotransferase (AST), and lipopolysaccharides, while increased the HDL-cholesterol content and the activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), lipoprotein lipase (LPL), and hepatic lipase (HL) in the serum of hyperlipidemic rats fed with the extract.…”

Section: Cardioprotective Effectsmentioning

confidence: 57%

“…They also improved the activity of SOD and in liver tissues, which inhibited the formation of MDA [168]. On the other hand, Abulizi et al [173] investigated the possibility of using aqueous extracts of C. oblonga in the treatment of atherosclerosis. They concluded that the extracts could improve the degree of aortic injury and hemodynamic indices, regulate blood lipid levels, and improve liver function in rats with atherosclerosis.…”

Section: Cardioprotective Effectsmentioning

confidence: 99%

Quinces (Cydonia, Chaenomeles and Pseudocidonia) as Less Distinguishable Medicinal Fruits of the Rosaceae Family. Current State of Knowledge on Properties and Use

Kostecka-Gugała

2023

Preprint

View full text Add to dashboard Cite

In recent years, the evaluation of many plant-derived compounds as potential new drugs or functional foods has become an active research topic. The characteristics of quinces of the genera Cydonia, Chaenomeles and Pseuocydonia are largely similar, which is why these fruits are often confused. Although they have been appreciated in Asia for centuries as a valuable component of local ethnomedicine, they are less known in Western countries and scientific knowledge about their health benefits remains fragmentary. This literature review presents the bioactive compounds of these fruits with special emphasis on antioxidants. Most space has been devoted to the presentation of the biological activities and potential medical applications of the fruits due to their antioxidant, anti-inflammatory, anticancer, cardioprotective and antidiabetic effects.

show abstract

“…It has been reported that VEGFA affects the development of AS by regulating lipid metabolism [ 30 ] and endothelial function [ 31 ]. Moreover, CTNNB1, MMP9, and EGFR have been shown to regulate AS by affecting the formation and stability of plaques through antioxidation and apoptosis inhibition [ 32 , 33 ]. Molecular docking is an important technique for discovering new medicines and improving existing drugs.…”

Section: Discussionmentioning

confidence: 99%

Network pharmacology and in vivo evidence of the pharmacological mechanism of geniposide in the treatment of atherosclerosis

Ma,

Dong,

et al. 2024

BMC Complement Med Ther

View full text Add to dashboard Cite

Background Atherosclerosis (AS) is a fundamental pathological state in various cardiovascular diseases. Geniposide, which is the main active component of Gardenia jasminides, is effective against AS. However, the underlying molecular mechanisms remain unclear. Here, we sought to elucidate them. Methods The targets of AS and geniposide were collected from online public databases. The potential mechanism of Geniposide in treating AS was predicted by constructing a protein–protein interaction (PPI) network and conducting Gene Ontology (GO) and Kyoto Encyclopaedia of Genes and Genomes (KEGG) pathway enrichment analyses. Hub proteins and core pathways were verified by molecular docking and in vivo experiments. Moreover, the effect of geniposide on AS was assessed by measuring the atherosclerotic plaque area in the thoracic aorta of mice. ApoE−/− mice were used to establish AS models and randomly divided into different groups. Two different doses of geniposide were administered to the mice. Hematoxylin and eosin (HE) staining was performed to evaluate the effects of geniposide on AS. Oil Red O and Sirius Red staining were used to evaluate plaque stability. The protein expression of key markers involved in the signalling pathways was examined using western blotting and immunofluorescence. Results A total of 239 active targets, 3418 AS-related disease targets, and 129 overlapping targets were identified. Hub genes were detected, and molecular docking revealed that geniposide strongly interacted with hub proteins (AKT1, VEGFA, CTNNB1, MMP9, and EGFR). Moreover, 109 signalling pathways, including the Rap1 signalling pathway, were identified using enrichment analysis. The results of in vivo experiments demonstrated that geniposide reduced body weight and blood lipid levels, alleviated the formation of atherosclerotic plaques, enhanced plaque stability, and inhibited inflammation, at least partially, by activating the Rap1/PI3K/Akt signalling pathway in ApoE−/− mice. Conclusion Geniposide can alleviate AS and enhance the stability of atherosclerotic plaques by regulating the Rap1/PI3K/Akt signalling pathway.

show abstract

Quince extract resists atherosclerosis in rats by down-regulating the EGFR/PI3K/Akt/GSK-3β pathway

Cited by 16 publications

References 32 publications

Recombinant hirudin attenuates pulmonary hypertension and thrombosis in acute pulmonary embolism rat model

Recombinant hirudin attenuates pulmonary hypertension and thrombosis in acute pulmonary embolism rat model

Quinces (Cydonia, Chaenomeles and Pseudocidonia) as Less Distinguishable Medicinal Fruits of the Rosaceae Family. Current State of Knowledge on Properties and Use

Network pharmacology and in vivo evidence of the pharmacological mechanism of geniposide in the treatment of atherosclerosis

Contact Info

Product

Resources

About