ArticleWorld journal of gastroenterology2008
Effects of ethanol on insulin-like growth factor-I system in primary cultured rat hepatocytes: implications of JNK1/2 and alcoholdehydrogenase.
Article in World journal of gastroenterology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 8 citations in OpenAlex.
- Role of Alcohol Oxidative Metabolism in Its Cardiovascular and Autonomic Effects.Advances in experimental medicine and biology · 2019Review
- Role of rostral ventrolateral medullary ERK/JNK/p38 MAPK signaling in the pressor effects of ethanol and its oxidative product acetaldehyde.Alcoholism, clinical and experimental research · 2013Article
- Alcohol consumption impairs hepatic protein trafficking: mechanisms and consequences.Genes & nutrition · 2010Article
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo evaluate the effects of ethanol on the insulin-like growth factor-I (IGF-I) system involved in c-Jun N-terminal kinase (JNK1/2) and alcoholdehydrogenase (ADH) activity in primary cultured rat hepatocytes.
methodsHepatocytes isolated from male Sprague-Dawley rats were incubated with various concentrations of ethanol for different durations of time. The cells were pretreated with SP600125 (10 mumol/L) and 4-MP (200 mumol/L), and then treated with ethanol (200 mmol/L). We then measured IGF-I secretion, IGF-I mRNA expression, cell viability and JNK1/2 activity by radioimmunoassay, RT-PCR, MTT assay and Western blot, respectively (n = 6).
resultsEthanol induced the activity of phospho (p)-JNK1/2, reaching a maximum at 60 min and then decreasing at 180 min. The effects of ethanol on the IGF-I system were increased at 60 min (secretion: 7.11 +/- 0.59 ng/mg protein vs 4.91 +/- 0.51 ng/mg, mRNA expression: 150.2% +/- 10.2% vs 101.5% +/- 11.3%, P = 0.045) and then decreased at 180 min (secretion: 3.89 +/- 0.25 ng/mg vs 5.4 +/- 0.54 ng/mg protein; mRNA expression: 41.5% +/- 10.4% vs 84.7% +/- 12.1%, P = 0.04), however cell viability was decreased in a dose- and time-dependent manner. SP600125 blocked the ethanol-induced changes (at 60 min). Additionally, 4-methylpyrazole prevented the ethanol-induced decreases in the IGF-I system, cell viability and p-JNK1/2 activity (at 180 min).
conclusionThis study suggests that ethanol-induced p-JNK1/2 activation is associated with the IGF-I system and cell viability in hepatocytes. Furthermore, alcohol dehydrogenase is involved in the relationship between ethanol-induced inactivation of p-JNK1/2 and the changes of the IGF-I system and cell viability.
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