Maltol attenuates polystyrene nanoplastic-induced enterotoxicity by promoting AMPK/mTOR/TFEB-mediated autophagy and modulating gut microbiota

Jin, Ming-hui; Hu, Jun‐Nan; Zhang, Ming; Meng, Ziqiang; Shi, Guo‐Ping; Wang, Zi; Li, Wei

doi:10.1016/j.envpol.2023.121202

Cited by 15 publications

(8 citation statements)

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“…26 A previous study revealed a connection between lysosomal dysfunction, impaired degradation of autophagic substrates, and intestinal damage. 27 Dong et al demonstrated that blocking mitochondrial disruption by improving lysosomal integrity ameliorates intestinal damage. 28 Our findings revealed that the DEPs were enriched in lysosome-associated GO and signaling pathways.…”

Section: ■ Resultsmentioning

confidence: 99%

“…Lysosomes play a crucial role in cellular autophagy, which is closely associated with intestinal dysfunction . A previous study revealed a connection between lysosomal dysfunction, impaired degradation of autophagic substrates, and intestinal damage . Dong et al demonstrated that blocking mitochondrial disruption by improving lysosomal integrity ameliorates intestinal damage .…”

Section: Discussionmentioning

confidence: 99%

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Integrated Transcriptome and Proteome Analyses of β-Conglycinin-Induced Intestinal Damage in Piglets

Li,

Zheng,

Yin

et al. 2024

J. Agric. Food Chem.

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β-conglycinin (β-CG) induces intestinal damage in piglets; however, its regulatory mechanisms are not fully understood. This study aimed to investigate the molecular mechanisms by which β-CG regulates intestinal injury in piglets through downstream genes and proteins. Our findings revealed that β-CG significantly reduced villus height while increasing the crypt depth. In addition, we analyzed the transcriptome and proteome of jejunum tissues after the β-CG treatment. In total, 382 differentially expressed genes (DEGs) and 292 differentially expressed proteins (DEPs) were identified between the treatment and the control groups. The expression levels of DEGs and DEPs were validated by using quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting, respectively. The findings revealed a consistent correlation between their expression levels and transcriptomic and proteomic data. In addition, Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses of DEGs and DEPs revealed their enrichment in oxidation-related GOs, as well as in lysosome-related pathways. A protein−protein interaction (PPI) regulatory network was constructed based on the DEPs. The integration of transcriptomic and proteomic analyses identified six genes that were significantly different at both the transcript and the protein levels. This study provides valuable insights into the molecular mechanisms underlying β-CG-induced intestinal injury in piglets.

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Section: ■ Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Integrated Transcriptome and Proteome Analyses of β-Conglycinin-Induced Intestinal Damage in Piglets

Li,

Zheng,

Yin

et al. 2024

J. Agric. Food Chem.

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“…To explore the potential liver toxicity of Np exposure, we selected 100 and 150 mg/kg for the study based on previous literature reports. 28 The results showed that there was no significant difference in ALT and AST among all groups, indicating that Nps could not affect the serum levels of transaminases at either a dose of 100 or 150 mg/kg (Figure 2A). However, the western blotting analysis results showed that Nps increased the release of apoptotic factors in the liver, impaired mitochondrial autophagy via the PINK1/Parkin pathway, and perturbed the redox equilibrium of the NOX4/Nrf2 axis.…”

Section: Establishment Of Animal and Cell Models Of Livermentioning

confidence: 93%

Nanoplastic-Induced Liver Damage Was Alleviated by Maltol via Enhancing Autophagic Flow: An In Vivo and In Vitro Study

Liang,

Wang,

Huo

et al. 2024

J. Agric. Food Chem.

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In recent years, there has been a growing concern regarding health issues arising from exposure to nanoplastics (Nps) in the natural environment. The Nps bioaccumulate within the body via the circulatory system and accumulate in the liver, resulting in damage. Previous studies have demonstrated that maltol, derived from red ginseng (Panax ginseng C.A. Meyer) as a Maillard product, exhibits hepatoprotective effects by alleviating liver damage caused by carbon tetrachloride or cisplatin. In order to explore the specific mechanism of maltol in improving hepatotoxicity induced by Nps, mice exposed to 100 mg/kg Nps were given maltol at doses of 50 and 100 mg/kg, respectively. The results showed that Nps induced an increase in the levels of liver apoptotic factors BAX and cytochrome c, a decrease in the levels of the autophagy key gene LC3 II/I, and an increase in P62. It also caused oxidative stress by affecting the Nrf2/HO-1 pathway, and a decrease in GPX4 protein expression suggested the occurrence of ferroptosis. However, treatment with maltol significantly improved these changes. In addition, maltol (2, 4, and 8 μM) also protected human normal liver L02 cells from Np (400 μg/mL)-induced damage. Our data suggest that maltol could ameliorate Np-induced L02 cytotoxicity by reducing autophagy-dependent oxidative stress, exhibiting similar protective effects in vitro as in vivo. This study helps shed light on the specific molecular mechanism of Np-induced hepatotoxicity. For the first time, we studied the protective effect of maltol on Np-induced liver injury from multiple perspectives, expanding the possibility of treatment for diseases caused by environmental pollutants.

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“…The autophagy marker LC3 II co-localized with fluorescence labelled nPs in cytoplasmic regions [ 116 ]. Additionally, mice exposed to 100 mg/kg of PS particles displayed interrupted degradation of autophagic substrates [ 117 ]. The interference of accumulated PS particles was confirmed by the colocalization of autophagy markers LC3 II and P62 in mouse embryonic fibroblasts [ 118 ].…”

Section: Autophagy Modulating Effects Of Nps: Autophagy Flux or Blockadementioning

confidence: 99%

The impact of nanomaterials on autophagy across health and disease conditions

Florance,

Cordani,

Pashootan

et al. 2024

Cell. Mol. Life Sci.

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Autophagy, a catabolic process integral to cellular homeostasis, is constitutively active under physiological and stress conditions. The role of autophagy as a cellular defense response becomes particularly evident upon exposure to nanomaterials (NMs), especially environmental nanoparticles (NPs) and nanoplastics (nPs). This has positioned autophagy modulation at the forefront of nanotechnology-based therapeutic interventions. While NMs can exploit autophagy to enhance therapeutic outcomes, they can also trigger it as a pro-survival response against NP-induced toxicity. Conversely, a heightened autophagy response may also lead to regulated cell death (RCD), in particular autophagic cell death, upon NP exposure. Thus, the relationship between NMs and autophagy exhibits a dual nature with therapeutic and environmental interventions. Recognizing and decoding these intricate patterns are essential for pioneering next-generation autophagy-regulating NMs. This review delves into the present-day therapeutic potential of autophagy-modulating NMs, shedding light on their status in clinical trials, intervention of autophagy in the therapeutic applications of NMs, discusses the potency of autophagy for application as early indicator of NM toxicity. Graphical Abstract

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Maltol attenuates polystyrene nanoplastic-induced enterotoxicity by promoting AMPK/mTOR/TFEB-mediated autophagy and modulating gut microbiota

Cited by 15 publications

References 46 publications

Integrated Transcriptome and Proteome Analyses of β-Conglycinin-Induced Intestinal Damage in Piglets

Integrated Transcriptome and Proteome Analyses of β-Conglycinin-Induced Intestinal Damage in Piglets

Nanoplastic-Induced Liver Damage Was Alleviated by Maltol via Enhancing Autophagic Flow: An In Vivo and In Vitro Study

The impact of nanomaterials on autophagy across health and disease conditions

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