ArticleFrontiers in pharmacology2025
The selective ERβ agonist AC 186 reduces polyinosinic:polycytidylic acid (poly I:C)-induced inflammatory responses in BEAS-2B lung epithelial cells.
Article in Frontiers in pharmacology, 2025. 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.
- Comparative Effects of Flurbiprofen and Benzydamine on COX-2/PGEInternational journal of molecular sciences · 2026Article
- Exosomal lncRNA DLEU2 aggravates inflammatory injury and apoptosis in pediatric viral pneumonia via the miR-330-5p.Hereditas · 2026Article
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Abstract
Background: Acute respiratory distress syndrome (ARDS) is characterised by inflammation with the accompanying release of pro-inflammatory cytokines. AC186 is an oestrogen receptor agonist, which has shown anti-inflammatory activity. This study investigated effects of AC186 on poly I:C-induced inflammation in human bronchial epithelial (BEAS-2B) cells. Methods: Supernatants from poly I:C-stimulated BEAS-2B cells treated with AC186 (1.25, 2.5 and 5 µM) were analysed for levels of tumour necrosis factor-alpha (TNFα), interleukins-6 (IL-6), -1β (IL-1β) and -8 (IL-8), using ELISA. Protein expression of phospho-p65 NF-κB was evaluated using Lumit Results: AC186 produced significant (p < 0.05) reduction in elevated levels of TNFα, IL-6, IL-1β and IL-8 in BEAS-2B cells, in comparison with poly I:C stimulation alone. Increased phosphorylation of p65 was significantly (p < 0.01) reduced in the presence of AC186 (2.5 and 5 µM), while nuclear localisation of p65, as well as DNA binding and transactivation were blocked with 2.5 and 5 µM of the compound. AC186 (2.5 and 5 µM) reduced protein levels of both NLRP3 inflammasome and caspase-1, as well as caspase-1 activity. Co-administration of ICI 182780 (10 nM) with AC186 (5 μM) prior to stimulation with poly I:C resulted in higher levels of TNFα and IL-6 secretion, compared to AC186 pre-treatment alone. Following incubation of AC186 (2.5 and 5 μM) with poly I:C-stimulated BEAS-2B cells for 72 h, there was significant improvement in viability as well as reduction in caspase 3/7 activity, in comparison with poly I:C alone. Conclusion: These results suggest that AC-186 produced anti-inflammatory activity in poly I:C-stimulated BEAS-2 cells, through mechanisms involving inhibition of NF-κB and NLRP3/caspase-1/IL-1β activation. AC186 also protected BEAS-2B cells against poly I:C-mediated apoptosis and death suggesting that this compound have potentials in reducing inflammatory events associated with ARDS caused by viral infections.
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