ArticleLipids in health and disease2014
Linoleate appears to protect against palmitate-induced inflammation in Huh7 cells.
Article in Lipids in health and disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 20 citations in OpenAlex.
- Physiologically relevant media are associated with overlapping metabolic responses in primary human hepatocytes and Huh7 cells.Physiological reports · 2026Article
- Hepatocyte Models for Metabolic Dysfunction-Associated Steatotic Liver Disease: A Comparative Analysis of Non-HepG2 Cell Models.International journal of molecular sciences · 2026Review
- EZH2-Mediated H3K27 Trimethylation in the Liver of Mice Is an Early Epigenetic Event Induced by High-Fat Diet Exposure.Nutrients · 2024Article
- The antioxidant barrier, oxidative/nitrosative stress, and protein glycation in allergy: from basic research to clinical practice.Frontiers in immunology · 2024Review
- Phytochemical profiles of edible flowers of medicinal plants ofFood science & nutrition · 2021Article
- Modifying nutritional substrates induces macrovesicular lipid droplet accumulation and metabolic alterations in a cellular model of hepatic steatosis.Physiological reports · 2020Article
- Free fatty acid-based low-impedance liver image: a characteristic appearance in nonalcoholic steatohepatitis (NASH).European radiology experimental · 2020Article
- Molecular mechanisms of lipotoxicity and glucotoxicity in nonalcoholic fatty liver disease.Metabolism: clinical and experimental · 2016Review
- Palmitate-induced Regulation of PPARγ via PGC1α: a Mechanism for Lipid Accumulation in the Liver in Nonalcoholic Fatty Liver Disease.International journal of medical sciences · 2016Article
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5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPolyunsaturated fatty acids (PUFAs) may protect against metabolic diseases. Although the benefits of the n-3 family of PUFA have been well investigated in nonalcoholic steatohepatitis (NASH), little is known about the effect of the n-6 family. This study examined the effect of linoleate, a member of the n-6 family, on regulation of the palmitate-induced inflammatory cytokine interleukin-8 (IL8) in hepatocytes.
methodsHuh7 cells and HepG2 cells were cultured with and without free fatty acid treatment (palmitate and linoleate, alone or in combination, 100-1000 μM). Inflammatory pathways, lipid accumulation, apoptosis and cell viability were monitored.
resultsDose- and time-related changes of IL8 mRNA expression were examined and 9 h treatment with 500 μM palmitate showed the greatest elevation of IL8. Co-treatment with 500 μM palmitate and 400 μM linoleate significantly suppressed IL8 production below that with palmitate alone in both cells (both mRNA and protein). A quantitative measurement for lipid accumulation showed no significant difference between palmitate-treated cells (1.69 ± 0.21), linoleate-treated cells (1.61 ± 0.16) and palmitate and linoleate-treated cells (1.73 ± 0.22, NS, n = 7). The co-treatment with 400 μM linoleate inhibited phospho-c-Jun N-terminal kinase (pJNK) activation and IkBα reduction caused by 500 μM palmitate treatment. Treatment with 400 μM linoleate alone led to IL8 production (5.48 fold change), similar to co-treatment, with no influence on the expression of pJNK/IkBα. The cell viability was similar between treatment with 500 μM palmitate and with both 500 μM palmitate and 400 μM linoleate, showing no significant changes in the expression of cleaved caspase-3.
conclusionsLinoleate is a potent regulator of the proinflammatory cytokine IL8 via the JNK and nuclear factor kappa B pathways that are involved in the pathophysiology of NASH, suggesting a future recommendation of dietary management.
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