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Le Carbone prevents liver damage in non-alcoholic steatohepatitis-hepatocellular carcinoma mouse model via AMPKα-SIRT1 signaling pathway activation. | LitMetric

AI Article Synopsis

  • Le Carbone (LC) is a dietary supplement made from activated charcoal and is investigated for its potential to protect against liver damage in a specific mouse model of non-alcoholic steatohepatitis-hepatocellular carcinoma (NASH-HCC).
  • The study involved administering LC to NASH mice and analyzing its effects on liver health, showing improvements in histopathology and liver enzyme levels.
  • LC treatment was found to restore key metabolic protein expressions that were depressed in NASH mice, suggesting it may work by enhancing the AMPK-SIRT1 signaling pathway to mitigate liver damage.

Article Abstract

Le Carbone (LC), a fiber-enriched activated charcoal dietary supplement, claimed to be effective against inflammation associated with colitis, trimethylaminuria, and sclerosis. The study aimed to investigate the underlying mechanisms of LC to protect liver damage and its progression in non-alcoholic steatohepatitis-hepatocellular carcinoma (NASH-HCC) mice. To induce this model, C57BL/6J male baby mice were injected with a low-dose of streptozotocin and fed with a high-fat diet (HFD) 32 during 4 weeks-16 weeks of age. The LC suspension was administered orally at a dose of 5 mg/mouse/day started at the age of 6 weeks and continued until 16 weeks of age along with HFD32 feeding. At the end of the experiment, serum and liver tissues were collected for the biochemical, histological, and molecular analysis. We found that LC suspension improved the histopathological changes, serum aminotransferases in NASH mice. The hepatic expression of metabolic proteins, p-AMPKα and sirtuin 1, and proteins responsible for β-oxidation of fatty acids, peroxisome proliferator-activated receptor (PPAR) γ coactivator-α, PPARα were significantly repressed in NASH mice. LC treatment markedly restored these expressions. LC treatment significantly reduced the hepatic proteins expressions of PPARγ, tissue inhibitor of metalloproteinases 4, p47phox, p-JNK, p-ERK1/2, glypican-3, and prothrombin in NASH mice. Our findings demonstrate that LC prevents the liver damage and progression of NASH, possibly by enhancing the AMPK-SIRT1 signaling pathway.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7803657PMC
http://dx.doi.org/10.1016/j.heliyon.2020.e05888DOI Listing

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