2019
DOI: 10.1177/0960327119895811
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Effects of quercetin on cadmium-induced toxicity in rat urine using metabonomics techniques

Abstract: This study aimed to analyse the protective effects of quercetin on the toxicity of cadmium (Cd) using metabonomics techniques. Sixty male Sprague–Dawley rats were randomly divided into six groups ( n = 10): control group (C), low-dose quercetin-treated group (Q1; 10 mg/kg bw/day), high-dose quercetin-treated group (Q2; 50 mg/kg bw/day), Cd-treated group (D; 4.89 mg/kg bw/day), low-dose quercetin plus Cd-treated group (DQ1) and high-dose quercetin plus Cd-treated group (DQ2). The rats continuously received quer… Show more

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Cited by 8 publications
(4 citation statements)
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“…A previous study of the protective effect of quercetin against cadmium toxicity found that the concentration of lysopc(18:2(9z,12z)) in the cadmium-treated group increased. Additionally, its intensity in the high-dose quercetin plus a cadmium-treated group showed a reversible change compared with the cadmium-treated group, which suggested its protective effect against cadmium toxicity by regulating lysopc(18:2(9Z, 12Z)) [ 43 ]. The methanol extract (DBME) suppressed intracellular ROS formation and downregulated LPS-induced iNOS, COX-2, and TNF expression, which suggested its potential as an anti-inflammatory agent.…”
Section: Discussionmentioning
confidence: 99%
“…A previous study of the protective effect of quercetin against cadmium toxicity found that the concentration of lysopc(18:2(9z,12z)) in the cadmium-treated group increased. Additionally, its intensity in the high-dose quercetin plus a cadmium-treated group showed a reversible change compared with the cadmium-treated group, which suggested its protective effect against cadmium toxicity by regulating lysopc(18:2(9Z, 12Z)) [ 43 ]. The methanol extract (DBME) suppressed intracellular ROS formation and downregulated LPS-induced iNOS, COX-2, and TNF expression, which suggested its potential as an anti-inflammatory agent.…”
Section: Discussionmentioning
confidence: 99%
“…41 Also, the protective effect of QUR against CdCl 2 induced liver, heart, and renal damage has been previously described and attributed to scavenging ROS, chelating of transition metals (i.e., Fe 2+ and Cu 2+ ), and upregulation of GSH and other antioxidant enzymes including SOD and catalase (CAT). 39,40 Also, QUR prevented hepatic inflammation, lipid deposition, and fibrosis in mice and rats with NAFLD by suppressing hepatic stellate cells (HSC) activation, ROS generation, the activation of NF-κB, the expression of TGF-β1/smad3/collagen I/III, and SREBP1a and improving SOD and CAT expression. [33][34][35][36]58,59 Despite these effects, the precise regulatory mechanism(s) underlying these pathological processes exerted by CdCl 2 and the protective pathways afforded by QUR still not clear.…”
Section: Discussionmentioning
confidence: 99%
“…Interestingly, Nrf2 also decreased in the livers of CdCl 2 -treated rats of this study which supports other previous reports. 40 In fact, with limited explanation, previous studies have shown that Nrf2 is an independent factor that inhibits hepatic lipid accumulation and fibrosis by suppressing SREBP1/2 and TGF-β1 signaling and concomitant activation of PPARα. [66][67][68] Therefrom, it could be possible that Nrf2 is the central key player mediating the activation or F I G U R E 9 A graphical abstract demonstrating the possible mechanisms by which cadmium chloride (CdCl 2 ) induces and quercetin (QUR) prevents CdCl2-induced hepatic steatosis and fibrosis.…”
Section: Discussionmentioning
confidence: 99%
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