Lycopene attenuates <scp>d</scp>-galactose-induced insulin signaling impairment by enhancing mitochondrial function and suppressing the oxidative stress/inflammatory response in mouse kidneys and livers

Wang, Jia; Li, Ting; Li, Mengling; Shi, Dongxing; Tan, Xiao Di; Qiu, Fubin

doi:10.1039/d2fo00706a

Cited by 8 publications

(5 citation statements)

References 43 publications

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“…Lycopene is a diverse biologically active antioxidant and anti-inflammatory agent that has been extensively studied in various disease models, such as arteriosclerosis, diabetes, and cancer [11]. A study shows that the lycopene diet can improve the kidney's antioxidant capacity by activating Nrf2 expression [21]. Nrf2 is a major transcription factor that regulates cellular oxidative stress responses, controls the primary defense mechanism against reactive oxygen species-induced tissue damage, and induces the expression of cellular inflammatory cytokines, including IL-β, IL-6, and TNF-a [22,23].…”

Section: Discussionmentioning

confidence: 99%

Lycopene-Loaded Bilosomes Ameliorate High-Fat Diet-Induced Chronic Nephritis in Mice through the TLR4/MyD88 Inflammatory Pathway

Liu

Wang

et al. 2022

Foods

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Chronic kidney disease caused by a high-fat diet (HFD)-induced metabolic syndrome has received widespread attention. Lycopene has a wide range of biological activities and can improve a variety of chronic diseases through anti-inflammatory effects. In this study, HFD-fed mice were used as a metabolic syndrome model to evaluate the protective effect of lycopene in a sustained-release vehicle (bilosomes) in the small intestine against renal injury and to determine whether the TLR4/MyD88 pathway and related metabolic pathways are involved in this process. The results showed that lycopene bilosomes alleviated HFD-induced kidney damage, as evidenced by lower serum urea nitrogen, creatinine, and uric acid levels. Histopathology studies showed that lycopene bilosomes attenuated HFD-induced tubular cell and glomerular injury. In addition, Elisa, RT-PCR, and Western blotting results showed that lycopene bilosomes also reduced the expression of inflammatory factors such as TLR4, MyD88, NF-kB, TNF-a, and IL-6 in mouse kidneys. The mechanism was to attenuate renal inflammatory response by inhibiting the TLR4/MyD88 inflammatory pathway. These findings suggested that lycopene can alleviate nephritis and metabolic disorders caused by HFD, inhibiting the TLR4/MyD88 inflammatory pathway and its downstream pro-inflammatory cytokines and further regulating the vitamin K metabolism, beta-alanine metabolism, and glutathione metabolism pathways to relieve chronic nephritis.

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Section: Discussionmentioning

confidence: 99%

Lycopene-Loaded Bilosomes Ameliorate High-Fat Diet-Induced Chronic Nephritis in Mice through the TLR4/MyD88 Inflammatory Pathway

Liu

Wang

et al. 2022

Foods

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“…Antioxidant properties of lycopene may contribute to the improvement of bone quality, as well as to the prevention of obesity-induced osteoporosis . LYC inhibits MAPK and nuclear factor kappa-B (NF-κB) pathways and attenuates renal and hepatic inflammatory responses . In terms of neuroprotection, mechanisms including oxidative stress, inflammation, apoptosis, and mitochondrial function recovery have been proved to mediate the neuroprotective effect of lycopene.…”

Section: Introductionmentioning

confidence: 99%

“…13 LYC inhibits MAPK and nuclear factor kappa-B (NF-κB) pathways and attenuates renal and hepatic inflammatory responses. 14 In terms of neuroprotection, mechanisms including oxidative stress, inflammation, apoptosis, and mitochondrial function recovery have been proved to mediate the neuroprotective effect of lycopene. However, whether LYC exerts a protective effect on DEHP-induced nephrotoxicity needs to be investigated.…”

Section: Introductionmentioning

confidence: 99%

Lycopene Attenuates Di(2-ethylhexyl) Phthalate-Induced Mitochondrial Damage and Inflammation in Kidney via cGAS–STING Signaling

Dai

Zhao

et al. 2022

J. Agric. Food Chem.

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Di(2-ethylhexyl) phthalate (DEHP) is a highly harmful and persistent environmental pollutant. Due to its unique chemical composition, it frequently dissolves and enters the environment to endanger human and animal health. Lycopene is a natural bioactive component that can potentially reduce the risk of environmental factor-induced chronic diseases. The present study sought to explore the role and underlying mechanism of lycopene (LYC) on DEHP-induced renal inflammatory response and apoptosis. In this study, mice were orally treated with LYC (5 mg/kg BW/day) and/or DEHP (500 or 1000 mg/kg BW/day) for 28 days. Our results indicated that LYC prevented DEHP-induced histopathological alterations and ultrastructural injuries, including decreased mitochondrial membrane potential (ΔΨm), PINK1/Parkin pathway-mediated mitophagy, and mitochondrial energetic deficit. When damaged mitochondria release mitochondrial DNA (mtDNA) into cytosol, LYC can alleviate inflammation and apoptosis caused by DEHP exposure by activating the cyclic GMP-AMP synthase-stimulator of interferon gene (cGAS–STING) signal pathway. Collectively, our data demonstrate that LYC can reduce mitophagy caused by DEHP exposure by activating the PINK1/Parkin pathway and then reduce renal inflammation and apoptosis through the cGAS–STING pathway.

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“…Some reports suggested that LYC could alleviate neurotoxicity and cognitive impairment caused by various toxicants exposure. 66,67 In our study, LYC was found to be effective in preventing DEHP-induced cognitive impairment by modulating ferroptosis. This finding provides new evidence and ideas for LYC to alleviate the cognitive dysfunction induced by phthalates.…”

Section: Discussionmentioning

confidence: 53%

Lycopene Prevents Phthalate-Induced Cognitive Impairment via Modulating Ferroptosis

Wang,

Li,

Cui

et al. 2023

J. Agric. Food Chem.

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phthalate (DEHP) is frequently used as a plasticizer in industrial and agricultural products. DEHP can cause severe neurotoxicity, such as impaired learning and memory function. Lycopene (LYC) as a carotenoid exerts excellent antioxidant capacity and therapeutic effects in neurodegenerative diseases. However, whether LYC can prevent the cognitive impairment induced by DEHP and the specific mechanisms are unclear. In the present study, the behavioral test results suggested that LYC alleviated the learning and memory impairment induced by DEHP. The histopathological data revealed that LYC attenuated DEHP-induced disordered arrangement of the neurons in the CA1 and CA3 regions of the hippocampus tissue. Moreover, LYC inhibited the occurrence of DEHP-induced ferroptosis via regulating iron metabolism, inhibiting lipid peroxidation, and activating the cysteine transporter and nuclear factor erythroid 2-related factor 2/heme oxygenase-1 (NrF2/HO-1) signaling pathway. Overall, the study contributes novel perspectives into the potential mechanisms of LYC preventing phthalate-induced cognitive impairment in the hippocampus.

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Lycopene attenuates d-galactose-induced insulin signaling impairment by enhancing mitochondrial function and suppressing the oxidative stress/inflammatory response in mouse kidneys and livers

Abstract: Lycopene (LYC) possesses bioactivity to improve the pathogenesis of several chronic diseases via antioxidant-associated mechanisms. The purpose of this study was to investigate whether LYC could attenuate D-galactose (D-gal)-induced mitochondrial...

Cited by 8 publications

References 43 publications

Lycopene-Loaded Bilosomes Ameliorate High-Fat Diet-Induced Chronic Nephritis in Mice through the TLR4/MyD88 Inflammatory Pathway

Lycopene-Loaded Bilosomes Ameliorate High-Fat Diet-Induced Chronic Nephritis in Mice through the TLR4/MyD88 Inflammatory Pathway

Lycopene Attenuates Di(2-ethylhexyl) Phthalate-Induced Mitochondrial Damage and Inflammation in Kidney via cGAS–STING Signaling

Lycopene Prevents Phthalate-Induced Cognitive Impairment via Modulating Ferroptosis

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