Crosstalk between unfolded protein response and Nrf2-mediated antioxidant defense in Di-(2-ethylhexyl) phthalate-induced renal injury in quail (Coturnix japonica)

Zhao, Yi; Du, Zheng-Hai; Talukder, Milton; Lin, Jianhua; Li, Xue-Nan; Cong, Zhen; Li, Jinlong

doi:10.1016/j.envpol.2018.07.080

Cited by 64 publications

(23 citation statements)

References 73 publications

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“…At present, the China National Environmental Monitoring Center, the United States Environmental Protection Agency, and the European Community has listed DEHP as a priority hazardous substance . Moreover, accumulating evidence has progressively indicated that DEHP exposure has many adverse effects on many tissues, such as spleen, liver, reproductive tract, heart, kidney, and lung (in primates and rodents). − A previous study reported that morphological and functional alterations of the spleen in animal models has suggested that DEHP exposure caused inflammatory responses . However, the DEHP causes spleen injury and the toxicity effects have not been extensively investigated.…”

Section: Introductionmentioning

confidence: 99%

Lycopene Ameliorates Di(2-ethylhexyl) Phthalate-Induced Pyroptosis in Spleen via Suppression of Classic Caspase-1/NLRP3 Pathway

Dai¹,

Li²,

Zhu³

et al. 2021

J. Agric. Food Chem.

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Lycopene (Lyc) as a natural antioxidant has attracted widespread attention. Di(2-ethylhexyl) phthalate (DEHP) can cause serious spleen injury in animals via the environment and food chain. For investigation of whether Lyc could alleviate DEHP-exerted pyroptosis in spleen through inhibiting the Caspase-1/NLRP3 pathway activation, 140 male mice were randomly divided into 7 groups: control group, vehicle control group, Lyc group (5 mg/kg BW/day), DEHP-exposed group (500 or 1000 mg/kg BW/day, respectively), and DEHP + Lyc groups by daily administration for 28 days. Pathological results showed that the supplementation of Lyc alleviated DEHP-induced inflammatory infiltration. Moreover, the addition of Lyc inhibited DEHP-induced Caspase-1, NLRP3, ASC, NF-κB, IL-1β, and IL-18 overexpression and GSDMD down-expression. These results indicate that Lyc could inhibit DEHP-induced Caspase-1-dependent pyroptosis and the inflammatory response. Taken together, the study provided new evidence that Lyc may be a strategy to mitigate spleen injury induced by DEHP.

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Section: Introductionmentioning

confidence: 99%

Lycopene Ameliorates Di(2-ethylhexyl) Phthalate-Induced Pyroptosis in Spleen via Suppression of Classic Caspase-1/NLRP3 Pathway

Dai¹,

Li²,

Zhu³

et al. 2021

J. Agric. Food Chem.

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“…Total RNA was extracted from homogenated kidney tissue and transcribed into cDNA as previously described . Analysis of the mRNA levels of AhR signaling pathway in the kidney was done by using quantitative real-time PCR (qRT-PCR).…”

Section: Methodsmentioning

confidence: 99%

“…Total RNA was extracted from homogenated kidney tissue and transcribed into cDNA as previously described. 51 Analysis of the mRNA levels of AhR signaling pathway in the kidney was done by using quantitative realtime PCR (qRT-PCR). The specific oligonucleotide primers for the AhR signaling pathway were listed in Table S2, designed by Oligo 7.22.…”

Section: ■ Materials and Methodsmentioning

confidence: 99%

Lycopene Preventing DEHP-Induced Renal Cell Damage Is Targeted by Aryl Hydrocarbon Receptor

Li¹,

Zhao²,

Wang³

et al. 2021

J. Agric. Food Chem.

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Di (2-ethylhexyl) phthalate (DEHP) is an environmentally persistent and bioaccumulative plasticizer. Accumulation of DEHP in the body can eventually cause kidney damage. As a type of natural carotenoid, lycopene (LYC) has a potential protective effect on renal cells, but the protective mechanism has not yet been elucidated. The major goal of this study was to see how effective LYC was at treating DEHP-induced nephrotoxicity in mice. ICR mice were treated with DEHP (500 mg/kg BW/day or 1000 mg/kg BW/day) or LYC (5 mg/kg BW/day) for 28 days. Through histopathology and ultrastructure, we found that LYC attenuated DEHP-induced renal tubular cell and glomerular damage. LYC relieved DEHP-induced kidney injury evidenced by lower levels of blood urea nitrogen (Bun), creatinine (Cre), and uric acid (Uric). Meanwhile, the reduced expression of kidney injury molecule-1 (Kim-1) also supported it. Notably, LYC can alleviate the activity or content of cytochrome P450 system (CYP450s) interfered with by DEHP. In addition, LYC treatment reduced nuclear accumulation of DEHP-induced aromatic hydrocarbon receptor (AhR) and AhR nuclear transporter (Arnt), and its downstream target genes such as cytochrome P450-dependent monooxygenase (CYP) 1A1, 1A2, and 1B1 expression significantly decreased to normal in the LYC treatment group. In summary, LYC can mediate the AhR/Arnt signaling system to prevent kidney toxicity in mice caused by DEHP exposure.

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“…These findings suggest that NRF2 activity is regulated through a complex transcriptional and post-translational network that makes it orchestrate the cell’s response and adaptation to various pathological stressors for homeostasis maintenance. In fact, previous reports showed that NRF2 exists at the center of a complex regulatory network and establishes NRF2 as a truly pleiotropic transcription factor, related to metabolic reprogramming, unfolded protein responses, autophagy, proteostasis, mitochondrial biogenesis, immunity, and inflammation [ 51 , 52 , 53 , 54 , 55 , 56 , 57 , 58 , 59 ] ( Figure 1 ).…”

Section: The Role Of Nrf2 In the Regulation Of Oxidative Stress And Its Role Other Than The Antioxidant Effectmentioning

confidence: 98%

The Role of NRF2 in Mycobacterial Infection

et al. 2021

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The incidence of pulmonary nontuberculous mycobacterial (NTM) infection is increasing worldwide, and its clinical outcomes with current chemotherapies are unsatisfactory. The incidence of tuberculosis (TB) is still high in Africa, and the existence of drug-resistant tuberculosis is also an important issue for treatment. To discover and develop new efficacious anti-mycobacterial treatments, it is important to understand the host-defense mechanisms against mycobacterial infection. Nuclear erythroid 2 p45-related factor-2 (NRF2) is known to be a major regulator of various antioxidant response element (ARE)-driven cytoprotective gene expressions, and its protective role has been demonstrated in infections. However, there are not many papers or reviews regarding the role of NRF2 in mycobacterial infectious disease. Therefore, this review focuses on the role of NRF2 in the pathogenesis of Mycobacterium tuberculosis and Mycobacterium avium infection.

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Crosstalk between unfolded protein response and Nrf2-mediated antioxidant defense in Di-(2-ethylhexyl) phthalate-induced renal injury in quail (Coturnix japonica)

Cited by 64 publications

References 73 publications

Lycopene Ameliorates Di(2-ethylhexyl) Phthalate-Induced Pyroptosis in Spleen via Suppression of Classic Caspase-1/NLRP3 Pathway

Lycopene Ameliorates Di(2-ethylhexyl) Phthalate-Induced Pyroptosis in Spleen via Suppression of Classic Caspase-1/NLRP3 Pathway

Lycopene Preventing DEHP-Induced Renal Cell Damage Is Targeted by Aryl Hydrocarbon Receptor

The Role of NRF2 in Mycobacterial Infection

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