ArticleInflammopharmacology2018
Diethylcarbamazine attenuates the expression of pro-fibrogenic markers and hepatic stellate cells activation in carbon tetrachloride-induced liver fibrosis.
Article in Inflammopharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Recent Advances in Research on Active Compounds Against Hepatic Fibrosis.Current medicinal chemistry · 2024Review
- Efficacy and Safety of Diethylcarbamazine in Treatment of Allergic Rhinitis: A Double Blind Randomised Controlled Trial.Indian journal of otolaryngology and head and neck surgery : official publication of the Association of Otolaryngologists of India · 2022Article
- Hepatoprotection ofVeterinary world · 2022Article
- Diethylcarbamazine as potential treatment of COVID-19 lung fibrosis.Medical hypotheses · 2022Article
- Human epididymis protein 4 (HE4) protects against cystic pulmonary fibrosis associated-inflammation through inhibition of NF-κB and MAPK singnaling.Genes & genomics · 2019Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND AND
aimWhile diethylcarbamazine citrate (DEC) displays important anti-inflammatory effects in experimental models of liver injury, the mechanisms of its action remain poorly understood. The aim of the present study was to investigate the fibrolytic potential of DEC.
methodsMice receive two injections of carbon tetrachloride (CCl
resultsThe expression of hepatic stellate cells (HSCs) activation markers, including smooth muscle α-actin (α-SMA), collagen I, transforming growth factor-β 1 (TGF-β1), matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of metalloproteinase-1 (TIMP-1) was assessed. The influence of DEC on the intracellular MAPK pathways of the HSCs (JNK and p38 MAPK) was also estimated. DEC inhibited HSCs activation measured as the production of α-SMA and collagen I. In addition, it down regulated the production of TGF-β1 and TIMP-1, and concomitantly increased MMP-2 activity. Furthermore, DEC significantly inhibited the activation of the JNK and p38 MAPK signaling pathways.
conclusionsIn conclusion, DEC significantly attenuated the severity of CCl
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