Protective effects of quercetin against oxidative stress induced by bisphenol-A in rat cardiac mitochondria

Vanani, Atefeh Raesi; Mahdavinia, Masoud; Shirani, Maryam; Alizadeh, Said; Dehghani, Mohammad Amin

doi:10.1007/s11356-020-08048-0

Cited by 24 publications

(14 citation statements)

References 51 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mitochondrial electron transport chain, endothelial nitric oxide synthase (eNOS), NADPH oxidase, xanthine oxidase (XO), as well as irradiation and environmental pollutants seems to induce oxidative stress and subsequently lead to lipid peroxidation, inflammation, and apoptosis (Sena, Leandro, Azul, Seica, & Perry, 2018). Several reports suggest that elevated levels of oxidative stress markers could have a fundamental role in the pathogenesis of cardiovascular disorders induced by BPA (Aboul Ezz et al, 2015; Han & Hong, 2016; Quagliariello et al, 2019; Vanani, Mahdavinia, Shirani, Alizadeh, & Dehghani, 2020) possibly through mitochondrial dysfunction and the oxidative damage of membrane phospholipids, proteins, and DNA (Aboul Ezz et al, 2015; Kabuto, Hasuike, Minagawa, & Shishibori, 2003). Malondialdehyde (MDA), an index of lipid peroxidation, has been currently considered as a potential biomarker for assessing oxidative stress in tissue injuries (Del Rio, Stewart, & Pellegrini, 2005).…”

Section: Discussionmentioning

confidence: 99%

Evaluation of green tea extract and epigallocatechin gallate effects on bisphenol A‐induced vascular toxicity in isolated rat aorta and cytotoxicity in human umbilical vein endothelial cells

Mohsenzadeh

Razavi

Imenshahidi

et al. 2020

Phytotherapy Research

View full text Add to dashboard Cite

This study was designed to assess bisphenol A (BPA)‐induced vascular toxicity, the effectiveness of green tea extract and epigallocatechin gallate (EGCG) against BPA toxicity, and possible underlying mechanisms. In isolated rat aorta, contractile and relaxant responses as well as malondialdehyde levels were evaluated. Cell viability and effects on the protein levels of apoptotic (bax, bcl2, and caspase‐3), autophagic (LC3), and cell adhesion molecules were calculated using the MTT method and western blotting in human umbilical vein endothelial cells (HUVECs). BPA increased aorta MDA levels (p < .0001) and decreased vascular responses to KCl [20 and 40 mM (p < .0001), 80 mM (p < .001)], phenylephrine [10−8, 10−6, and 10−5 M (p < .001), 10−7 and 10−4 M (p < .0001)], and acetylcholine [10−6 M (p < .01), 10−5 and 10−4 M (p < .0001)]. In HUVECs, BPA enhanced the levels of LC3A/B, bax/bcl2 ratio, cleaved caspase‐3, and vascular cell adhesion molecule‐1. Green tea extract, EGCG, and vitamin E co‐treatment with BPA diminished the toxic effects of BPA. These findings provide evidence that green tea extract and EGCG possess beneficial effects in preventing BPA‐induced vascular toxicity through increasing the antioxidant activities and the regulation of signaling pathways.

show abstract

Section: Discussionmentioning

confidence: 99%

Evaluation of green tea extract and epigallocatechin gallate effects on bisphenol A‐induced vascular toxicity in isolated rat aorta and cytotoxicity in human umbilical vein endothelial cells

Mohsenzadeh

Razavi

Imenshahidi

et al. 2020

Phytotherapy Research

View full text Add to dashboard Cite

show abstract

“…The results showed that quercetin supplementation significantly reduced levels of oxidative stress markers, suggesting a potential protective effect against oxidative damage. 31 Quercetin may help to protect cells from damage caused by harmful molecules called free radicals and also widen blood vessels, which can lower blood pressure and improve blood flow. 32 Quercetin has also been studied for its effects on vascular biology, particularly in relation to endothelial function and blood pressure regulation.…”

Section: Discussionmentioning

confidence: 99%

Quercetin attenuates angiotensin II‐induced proliferation of vascular smooth muscle cells and p53 pathway activation in vitro and in vivo

et al. 2023

View full text Add to dashboard Cite

Quercetin is an essential flavonoid mostly found in herbal plants, fruits, and vegetables, which exhibits anti‐hypertension properties. However, its pharmacological impact on angiotensin II (Ang II) induced the increase of blood pressure along with in‐depth mechanism needs further exploration. The present study pointed out the anti‐hypertensive role of quercetin and its comprehensive fundamental mechanisms. Our data showed that quercetin treatment substantially reduced the increase in blood pressure, pulse wave velocity, and aortic thickness of abdominal aorta in Ang II‐infused C57BL/6 mice. RNA sequencing revealed that quercetin treatment reversed 464 differentially expressed transcripts in the abdominal aorta of Ang II‐infused mice. Moreover, overlapping KEGG‐enriched signaling pathways identified multiple common pathways between the comparison of Ang II versus control and Ang II + quercetin versus Ang II. Likewise, these pathways included cell cycle as well as p53 pathways. Transcriptome was further validated by immunohistochemistry, indicating that quercetin treatment significantly decreased the Ang II‐induced expression of proliferating cell nuclear antigen (PCNA), cyclin‐dependent kinase‐4 (CDK4), and cyclin D1, while increased protein expression of p53, and p21 in abdominal aortic tissues of mice. In vitro, quercetin treatment meaningfully decreased the cell viability, arrested cell cycle at G0/G1 phase, and up‐regulated the p53 and p21 proteins expression, as well as down‐regulated the protein expression of cell cycle‐related markers, for example, CDK4, cyclin D1 in Ang II stimulated vascular smooth muscle cells (VSMCs). This study addresses pharmacologic and mechanistic perspectives of quercetin against Ang‐II‐induced vascular injury and the increase of blood pressure.

show abstract

“…Many studies have demonstrated quercetin's efficacy as a hypolipidemic and NAFLD protectant in animal experiments and clinical trials, making it a candidate for future pharmacological therapy against NAFLD 16,[21][22][23] . Additionally, liver inflammation and other pathophysiological processes, such as oxidative stress and energy consumption, are also targets of quercetin in NAFLD treatment 24,25 .…”

Section: Discussionmentioning

confidence: 99%

Quercetin Ameliorates Fatty Acid Oxidation in the Pathogenesis of NAFLD Based on Network Pharmacology and Molecular Docking

Zhu

Dai

Lin

et al. 2021

Preprint

View full text Add to dashboard Cite

The high-fat diet (HFD) has dramatically increased the prevalence of non-alcoholic fatty liver disease (NAFLD), such that it is the leading cause of chronic liver disease worldwide. With novel knowledge on pathogenesis of NAFLD, we illustrated molecular targets for pharmacologic and experimental approaches. Our study showed that quercetin was the valuable drug candidate, and the core targets such as PPARα, MCAD, LCAD, CPT1-L, CPT2 and FATP2 which participate in fatty acid oxidation were selected to perform further in vivo experiments based on network pharmacology and molecular docking technology. The effect was investigated in a high-fat diet-induced NAFLD male Sprague Dawley rat model by hepatic biochemical assays. Serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and γ-glutamyl transferase analyses assessed liver function. Liver tissues were collected for histological staining, quantitative real-time PCR and western blotting. Greatly, quercetin reduced hepatic lipid accumulation and inflammation, ameliorated pathological liver changes, and up-regulated the expression levels of hepatic effectors in fatty acid oxidation. The results suggest the potential of quercetin as a nutritional supplement to HFD-induced NAFLD. Furthermore, the antagonist and agonist of PPARα provided a reliable scientific basis that these above-mentioned effectors were activated by quercetin via the PPAR pathway.

show abstract

Protective effects of quercetin against oxidative stress induced by bisphenol-A in rat cardiac mitochondria

Cited by 24 publications

References 51 publications

Evaluation of green tea extract and epigallocatechin gallate effects on bisphenol A‐induced vascular toxicity in isolated rat aorta and cytotoxicity in human umbilical vein endothelial cells

Evaluation of green tea extract and epigallocatechin gallate effects on bisphenol A‐induced vascular toxicity in isolated rat aorta and cytotoxicity in human umbilical vein endothelial cells

Quercetin attenuates angiotensin II‐induced proliferation of vascular smooth muscle cells and p53 pathway activation in vitro and in vivo

Quercetin Ameliorates Fatty Acid Oxidation in the Pathogenesis of NAFLD Based on Network Pharmacology and Molecular Docking

Contact Info

Product

Resources

About