hepatoprotective effects of licochalcone b on carbon tetrachloride-induced liver toxicity in mice

Clicks: 404
ID: 235742
2016
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #402 of 2,056 articles by views in PloS one

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 2,056 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Objective(s): The objective of this study was to investigate the hepatoprotective effect of licochalcone B (LCB) in a mice model of carbon tetrachloride (CCl4)-induced liver toxicity. Materials and Methods: Hepatotoxicity was induced in mice by a single subcutaneous injection (SC) of CCl4. The LCB was administered orally once a day for seven days (PO) as pretreatment at three doses of 1, 5, and 25 mg/kg/day. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), glutathione disulfide (GSSG), C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA. The protein expression degrees of p38 mitogen activated protein kinases (p38) and nuclear factor-k-gene binding (NF-κB) were assayed by western blotting. Results: CCl4-induced hepatotoxicity was manifested by an increase in the levels of ALT, AST, MDA, IL-6, CRP, and TNF-ɑ, and a decrease in the SOD level and GSH/GSSG ratio in the serum. The histopathological examination of the liver sections revealed necrosis and inflammatory reactions. Pretreatment with LCB decreased the levels of ALT, AST, MDA, GSSG, IL-6, CRP, TNF-ɑ, and the protein expression of p38 and NF-κB, increased the level of SOD and GSH, and normalized the hepatic histo-architecture. Conclusion: LCB protected the liver from CCl4-induced injury. Protection may be due to inhibition of p38 and NFκB signaling, which subsequently reduced inflammation in the liver.
Objetivo(s): O objetivo deste estudo foi investigar o efeito hepatoprotetor da licochalcona B (LCB) em um modelo de toxicidade hepática induzida por tetracloreto de carbono (CCl4) em camundongos. Materiais e Métodos: A hepatotoxicidade foi induzida em camundongos por uma única injeção subcutânea (SC) de CCl4. A LCB foi administrada por via oral, uma vez ao dia, durante sete dias (VO) como pré-tratamento em três doses de 1, 5 e 25 mg/kg/dia. Os níveis de superóxido dismutase (SOD), malondialdeído (MDA), glutationa (GSH), dissulfeto de glutationa (GSSG), proteína C-reativa (PCR), fator de necrose tumoral-α (TNF-α), interleucina-6 (IL-6), alanina aminotransferase (ALT) e aspartato aminotransferase (AST) foram analisados por ELISA. Os níveis de expressão proteica das proteínas quinases ativadas por mitógenos p38 (p38) e do fator nuclear kappa B (NF-κB) foram avaliados por western blotting. Resultados: A hepatotoxicidade induzida por CCl4 manifestou-se por um aumento nos níveis de ALT, AST, MDA, IL-6, PCR e TNF-α, e por uma diminuição no nível de SOD e na razão GSH/GSSG no soro. O exame histopatológico dos cortes hepáticos revelou necrose e reações inflamatórias. O pré-tratamento com LCB reduziu os níveis de ALT, AST, MDA, GSSG, IL-6, PCR e TNF-α, bem como a expressão proteica de p38 e NF-κB, aumentou os níveis de SOD e GSH e normalizou a histoarquitetura hepática. Conclusão: A LCB protegeu o fígado contra a lesão induzida por CCl4. Essa proteção pode ser decorrente da inibição da sinalização de p38 e NF-κB, que subsequentemente reduziu a inflamação hepática.
Reference Key
teng2016iranianhepatoprotective Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Haifeng Teng;Meng Chen;Ansheng Chu;Haili Jiang;Jichun Han;Long Sun;Chao Feng;Ju Liu
Journal PloS one
Year 2016
DOI
10.22038/ijbms.2016.7474
URL
http://ijbms.mums.ac.ir/article_7474_d3ebb0790ba2d068b65ccb02e8a4688c.pdf
Keywords
antioxidant anti-inflammatory nf-κb hepatotoxicity carbon tetrachloride

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.