Lycopene attenuates AFB<sub>1</sub>-induced renal injury with the activation of the Nrf2 antioxidant signaling pathway in mice

Kobayashi, Yu; Zhang, Jian; Cao, Zheng; Ji, Qiang; Han, Yaling; Song, Miao; Lei, Lei; Li, Yanfei

doi:10.1039/c8fo01301b

Cited by 49 publications

(35 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…GSH-Px, SOD, CAT, and T-AOC are critical indicators for evaluating the capacity of the cellular antioxidant defense system [32,33]. An imbalance in oxidative stress defense leads to insufficient antioxidant responses and lipid peroxidation to generate MDA [31,34]. As mentioned, SCHPs-F1 increased the antioxidant defense parameters GSH-Px, SOD, CAT, and T-AOC and decreased levels of the lipid peroxidation marker MDA, thereby potentially alleviating oxidative stress of CTX-exposed kidneys.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

et al. 2020

View full text Add to dashboard Cite

The major component of the Solenocera crassicornis head protein hydrolysates-fraction 1 (SCHPs-F1) are low molecular weight peptides (MW < 1 kDa). In this study, we investigated the potential renoprotective effects of SCHPs-F1 in a cyclophosphamide (CTX) toxicity mouse model. In brief, 40 male mice were randomly divided into 5 groups and received either saline or 80 mg/kg body weight (BW) CTX by intraperitoneal injection for 5 days, followed by either saline or SCHPs-F1 (100, 200, and 400 mg/kg BW) by intragastric administration for 15 days. SCHPs-F1 treatment significantly reversed the CTX-induced decreases in the levels of blood urea nitrogen (BUN), creatinine (CRE), and cytochrome P450 (CYP450), as well as the renal histological lesions. Furthermore, the results indicated that SCHPs-F1 potentially alleviated CTX-induced nephrotoxicity through mitigating inflammatory responses, oxidative stress, and apoptosis status of the kidneys, as evidenced by decreased levels of malondialdehyde (MDA), interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ and increased levels of total antioxidant capacity (T-AOC), catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px). Moreover, overexpression of pro-apoptotic proteins pair B-cell lymphoma-2 (Bcl-2)-associated X (Bax)/Bcl-2, cysteinyl aspartate specific proteinase (caspase)-3 and caspase-9 in renal tissues were suppressed by treatment with SCHPs-F1. In addition, the protein levels of the antioxidant factor nuclear factor erythroid-2 related factor 2 (Nrf2) and the expression levels of its downstream target genes heme-oxygenase (HO-1), glutamate-cysteine ligase modifier subunit (GCLM) and NAD(P)H dehydrogenase (quinone) 1 (NQO-1) were stimulated by treatment with SCHPs-F1 in the CTX-induced renal injury model. Taken together, our data suggested that SCHPs-F1 could provide a novel potential strategy in mitigating the nephrotoxicity caused by CTX.

show abstract

Section: Discussionmentioning

confidence: 99%

Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

et al. 2020

View full text Add to dashboard Cite

show abstract

“…These results agree with the results of Abbas et al [36] who reported that lycopene ameliorates atrazine-induced oxidative damage in the adrenal cortex of male rats by activation of the RF/HO-1 pathway. Furthermore, Yu et al [37] reported that lycopene attenuates aflatoxin B1-induced renal injury with the activation of the RF antioxidant signaling pathway in mice. Therefore, it is highly suggested that lycopene-induced upregulation of antioxidant enzymes is mechanistically via activation of the RF pathway.…”

Section: Resultsmentioning

confidence: 99%

Effects of Pyrene on Human Liver HepG2 Cells: Cytotoxicity, Oxidative Stress, and Transcriptomic Changes in Xenobiotic Metabolizing Enzymes and Inflammatory Markers with Protection Trial Using Lycopene

Eldin

El‐Ghareeb

et al. 2019

BioMed Research International

View full text Add to dashboard Cite

Pyrene is one of the major polycyclic aromatic hydrocarbons formed during heat treatment of meat and in car exhausts; however, few studies have investigated pyrene-induced adverse effects on human cell lines. This study aimed at the investigation of pyrene-induced cytotoxicity and oxidative damage in human liver HepG2 cells at environmentally relevant concentrations. Pyrene-induced changes in mRNA expression of xenobiotic metabolizing enzymes (XMEs), xenobiotic transporters, antioxidant enzymes, and inflammatory markers were investigated using real-time PCR. As a protection trial, the ameliorative effects of lycopene, a carotenoid abundantly found in tomato, were investigated. The possible mechanisms behind such effects were examined via studying the co exposure effects of pyrene and lycopene on regulatory elements including the aryl hydrocarbon receptor (Air) and elytroid 2-related factor 2 (RF). The achieved results indicated that pyrene caused significant cytotoxicity at 50 n, with a clear production of reactive oxygen species (ROS) in a dose-dependent manner. Pyrene upregulated mRNA expression of phase I enzymes including CYP1A1, 1A2, and CYP1B1 and inflammatory markers including TNFα and Cox2. However, pyrene significantly downregulated phase II enzymes, xenobiotic transporters, and antioxidant enzymes. Interestingly, lycopene significantly reduced pyrene-induced cytotoxicity and ROS production. Moreover, lycopene upregulated detoxification and antioxidant enzymes, probably via its regulatory effects on Air- and RF-dependent pathways.

show abstract

“…Each sample was analyzed in triplicates and the mRNA expression of the target genes was analyzed by 2 −△△Ct method, following normalization with β-actin gene. Primer sequences of HDAC1 and β-actin genes are shown as follows: HDAC1, 5’-TGAAGCCTCACCGAATCCG-3’ and 5’-GGGCGAATAGAACGCAGGA-3’ ( Deng et al, 2020 ); β-actin, 5’-GTTGGAGCAAACATCCCCCA-3’ and 5’-ACGCGACCATCCTCCTC TTA-3’ ( Yu et al, 2018 ).…”

Section: Methodsmentioning

confidence: 99%

7-Hydroxycoumarin Attenuates Colistin-Induced Kidney Injury in Mice Through the Decreased Level of Histone Deacetylase 1 and the Activation of Nrf2 Signaling Pathway

et al. 2020

View full text Add to dashboard Cite

Colistin has been considered as the last line of defense against Gram-negative bacterial infections, however, the potential nephrotoxicity limited its clinical use. 7-Hydroxycoumarin (7-HC) possesses many beneficial pharmacological activities. This study aimed to investigate the nephroprotective effects of 7-HC against colistin-induced kidney injury. In vivo experiments showed that 7-HC alleviated kidney injury induced by colistin, as indicated by lower levels of serum neutrophil gelatinase-associated lipocalin, blood urea nitrogen and creatinine levels. Both in vivo and in vitro results demonstrated that 7-HC alleviated oxidative stress and apoptosis induced by colistin, as shown by decreased malondialdehyde levels, decreased caspase-3 and caspase-9 activities, and increased superoxide dismutase and catalase activities. We also found that colistin significantly induced histone deacetylase (HDAC) 1 expression that deacetylated histone 3 at Lys27 acetylation (H3K27AC) of Nrf2 promoter region and hence inhibiting Nrf2 signaling. 7-HC treatment restored histone acetylation at the Nrf2 promoter region and hence promoted Nrf2 expression. These results suggested that 7-HC alleviates colistin-induced renal injury and this effect was achieved by enhancement of renal antioxidant capacity with the decreased level of HDAC1 and the activation of Nrf2 signaling pathway.

show abstract

Lycopene attenuates AFB₁-induced renal injury with the activation of the Nrf2 antioxidant signaling pathway in mice

Abstract: Proposed renoprotection mechanism of LYC via enhancing renal antioxidant in AFB1-treated mice kidney. The → indicates activation or induction, and ⊣ indicates inhibition or blockade.

Cited by 49 publications

References 58 publications

Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

Effects of Pyrene on Human Liver HepG2 Cells: Cytotoxicity, Oxidative Stress, and Transcriptomic Changes in Xenobiotic Metabolizing Enzymes and Inflammatory Markers with Protection Trial Using Lycopene

7-Hydroxycoumarin Attenuates Colistin-Induced Kidney Injury in Mice Through the Decreased Level of Histone Deacetylase 1 and the Activation of Nrf2 Signaling Pathway

Contact Info

Product

Resources

About

Lycopene attenuates AFB1-induced renal injury with the activation of the Nrf2 antioxidant signaling pathway in mice

Abstract: Proposed renoprotection mechanism of LYC via enhancing renal antioxidant in AFB1-treated mice kidney. The → indicates activation or induction, and ⊣ indicates inhibition or blockade.

Cited by 49 publications

References 58 publications

Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

Protective Effect of Low Molecular Weight Peptides from Solenocera crassicornis Head against Cyclophosphamide-Induced Nephrotoxicity in Mice via the Keap1/Nrf2 Pathway

Effects of Pyrene on Human Liver HepG2 Cells: Cytotoxicity, Oxidative Stress, and Transcriptomic Changes in Xenobiotic Metabolizing Enzymes and Inflammatory Markers with Protection Trial Using Lycopene

7-Hydroxycoumarin Attenuates Colistin-Induced Kidney Injury in Mice Through the Decreased Level of Histone Deacetylase 1 and the Activation of Nrf2 Signaling Pathway

Contact Info

Product

Resources

About

Lycopene attenuates AFB₁-induced renal injury with the activation of the Nrf2 antioxidant signaling pathway in mice