ArticleActa pharmacologica Sinica2010
Antifibrotic effects of ZK14, a novel nitric oxide-donating biphenyldicarboxylate derivative, on rat HSC-T6 cells and CCl4-induced hepatic fibrosis.
Article in Acta pharmacologica Sinica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 12 citations in OpenAlex.
- Nitric oxide augments mesenchymal stem cell ability to repair liver fibrosis.Journal of translational medicine · 2012Article
- Predicting in vivo anti-hepatofibrotic drug efficacy based on in vitro high-content analysis.PloS one · 2011Article
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Authors and funding
4 authors at 1 institution in 1 country.
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Abstract
aimTo study the pharmacologic effect of ZK(14), a novel nitric oxide-donating biphenyldicarboxylate (DDB) derivative, on HSC-T6 cells and on CCl(4)-induced hepatic fibrosis.
methodsInhibition of HSC-T6 cell growth by ZK(14) was evaluated by MTT assay. The effect of ZK(14) on the percentage of HSC-T6 cells undergoing apoptosis was measured using Annexin-V/PI double-staining and TUNEL assay. Mitochondrial membrane potential (MMP) and caspase activities were tested. Hepatic fibrosis was induced in Sprague-Dawley rats by intraperitoneal injection with 14% CCl(4). Rats with hepatic fibrosis were randomly divided into four groups: model control, ZK(14) (20 mg/kg), ZK(14) (10 mg/kg) and DDB (5 mg/kg). Levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), hyaluronic acid (HA), type III collagen (PCIII), and nitric oxide (NO) were assessed, and liver samples were stained with hematoxylin-eosin. The NO level in cells treated with ZK(14) in vitro was also measured.
resultsThe effect of ZK(14) on HSC-T6 cell apoptosis was concentration- and time-dependent, with up to 50% of cells becoming apoptotic when exposed to 100 mumol/L ZK(14) for 18 h. ZK(14) treatment resulted in mitochondrial membrane depolarization and activation of caspases 3 and 9. At a dose of 20 mg/kg, ZK(14) significantly decreased serum transaminase (AST, ALT) activities and fibrotic index (HA, PCIII) levels and significantly inhibited fibrogenesis.
conclusionThese data indicate that ZK(14), a novel NO-donating DDB derivative, promotes HSC-T6 apoptosis in vitro through a signaling mechanism involving mitochondria and caspase activation and it inhibits CCl(4)-induced hepatic fibrosis in vivo. The results suggest that ZK(14) has potential therapeutic value in the treatment of hepatic fibrosis.
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