دورية أكاديمية
Oral bisphenol a worsens liver immune-metabolic and mitochondrial dysfunction induced by high-fat diet in adult mice: cross-talk between oxidative stress and inflammasome pathway
| العنوان: | Oral bisphenol a worsens liver immune-metabolic and mitochondrial dysfunction induced by high-fat diet in adult mice: cross-talk between oxidative stress and inflammasome pathway |
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| المؤلفون: | Pirozzi C., Lama A., Annunziata C., Cavaliere G., Ruiz-Fernandez C., Monnolo A., Comella F., Gualillo O., Stornaiuolo M., Mollica M. P., Raso G. M., Ferrante M. C., Meli R. |
| المساهمون: | Pirozzi, C., Lama, A., Annunziata, C., Cavaliere, G., Ruiz-Fernandez, C., Monnolo, A., Comella, F., Gualillo, O., Stornaiuolo, M., Mollica, M. P., Raso, G. M., Ferrante, M. C., Meli, R. |
| سنة النشر: | 2020 |
| المجموعة: | IRIS Università degli Studi di Perugia |
| مصطلحات موضوعية: | Inflammatory cytokines, Liver fibrosis, Mitochondrial respiratory capacity, NLRP3 inflammasome signaling pathway, Obesity, Reactive oxygen species, Toll-like receptor-4 |
| الوصف: | Lines of evidence have shown the embryogenic and transgenerational impact of bisphenol A (BPA), an endocrine-disrupting chemical, on immune-metabolic alterations, inflammation, and oxidative stress, while BPA toxic effects in adult obese mice are still overlooked. Here, we evaluate BPA’s worsening effect on several hepatic maladaptive processes associated to high-fat diet (HFD)-induced obesity in mice. After 12 weeks HFD feeding, C57Bl/6J male mice were exposed daily to BPA (50 μg/kg per os) along with HFD for 3 weeks. Glucose tolerance and lipid metabolism were examined in serum and/or liver. Hepatic oxidative damage (reactive oxygen species, malondialdehyde, antioxidant enzymes), and mitochondrial respiratory capacity were evaluated. Moreover, liver damage progression and inflammatory/immune response were determined by histological and molecular analysis. BPA amplified HFD-induced alteration of key factors involved in glucose and lipid metabolism, liver triglycerides accumulation, and worsened mitochondrial dysfunction by increasing oxidative stress and reducing antioxidant defense. The exacerbation by BPA of hepatic immune-metabolic dysfunction induced by HFD was shown by increased toll-like receptor-4 and its downstream pathways (i.e., NF-kB and NLRP3 inflammasome) amplifying inflammatory cytokine transcription and promoting fibrosis progression. This study evidences that BPA exposure represents an additional risk factor for the progression of fatty liver diseases strictly related to the cross-talk between oxidative stress and immune-metabolic impairment due to obesity. |
| نوع الوثيقة: | article in journal/newspaper |
| وصف الملف: | ELETTRONICO |
| اللغة: | English |
| العلاقة: | info:eu-repo/semantics/altIdentifier/pmid/33265944; info:eu-repo/semantics/altIdentifier/wos/WOS:000601803700001; volume:9; issue:12; firstpage:1; lastpage:14; numberofpages:14; journal:ANTIOXIDANTS; http://hdl.handle.net/11391/1517730Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85097148383; https://pubmed.ncbi.nlm.nih.gov/33265944Test/ |
| DOI: | 10.3390/antiox9121201 |
| الإتاحة: | https://doi.org/10.3390/antiox9121201Test http://hdl.handle.net/11391/1517730Test https://pubmed.ncbi.nlm.nih.gov/33265944Test/ |
| رقم الانضمام: | edsbas.DA2876D |
| قاعدة البيانات: | BASE |
| DOI: | 10.3390/antiox9121201 |
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