Long-term exposure to polychlorinated biphenyl 126 induces liver fibrosis and upregulates miR-155 and miR-34a in C57BL/6 mice.

Fernanda Torres Quitete, Ananda Vitória Silva Teixeira, Thamara Cherem Peixoto, Bruna Cadete Martins, Geórgia Correa Atella, Angela de Castro Resende, Daniela de Barros Mucci, Fabiane Martins, Julio Beltrame Daleprane
Author Information
  1. Fernanda Torres Quitete: Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro, Brazil.
  2. Ananda Vitória Silva Teixeira: Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro, Brazil.
  3. Thamara Cherem Peixoto: Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro, Brazil.
  4. Bruna Cadete Martins: Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro, Brazil.
  5. Geórgia Correa Atella: Medical Biochemistry Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
  6. Angela de Castro Resende: Department of Pharmacology, Rio de Janeiro State University, Rio de Janeiro, Brazil.
  7. Daniela de Barros Mucci: Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro, Brazil. ORCID
  8. Fabiane Martins: Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro, Brazil.
  9. Julio Beltrame Daleprane: Department of Basic and Experimental Nutrition, Rio de Janeiro State University, Rio de Janeiro, Brazil. ORCID

Abstract

Environmental pollutants, including polychlorinated biphenyls (PCBs), act as endocrine disruptors and impair various physiological processes. PCB 126 is associated with steatohepatitis, fibrosis, cirrhosis, and other hepatic injuries. These disorders can be regulated by microRNAs (miRNAs). Therefore, this study aimed to investigate the role of miRNAs in non-alcoholic fatty liver disease associated with exposure to PCB 126. Adult male C57BL/6 mice were exposed to PCB 126 (5 μmol/kg of body weight) for 10 weeks. The PCB group showed lipid accumulation in the liver in the presence of macro- and microvesicular steatosis and fibrosis with increased inflammatory and profibrotic gene expression, consistent with non-alcoholic steatohepatitis (NASH). PCB exposure also upregulated miR-155 and miR-34a, which induce the expression of proinflammatory cytokines and inflammation in the liver and reduce the expression of peroxisome proliferator-activated receptor α, which, in turn, impairs lipid oxidation and hepatic steatosis. Therefore, the present study showed that PCB 126 induced NASH via potential mechanisms involving miR-155 and miR-34a, which may contribute to the development of new diagnostic markers and therapeutic strategies.

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MeSH Term

Animals
MicroRNAs
Polychlorinated Biphenyls
Male
Mice, Inbred C57BL
Mice
Liver Cirrhosis
Up-Regulation
Liver
Non-alcoholic Fatty Liver Disease
Environmental Pollutants
Lipid Metabolism

Chemicals

MicroRNAs
Polychlorinated Biphenyls
MIRN34a microRNA, mouse
Mirn155 microRNA, mouse
3,4,5,3',4'-pentachlorobiphenyl
Environmental Pollutants

Word Cloud

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