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Área Científica » Trabalhos Premiados » EFFECTS OF ROSMARINIC ACID IN SUPRESSING RESPONSES CONTRIBUTING TO FIBROSIS IN TGF-BETA-STIMULATED TENON'S FIBROBLASTS

Código: P 058
Apresentação: Pôster
Área Técnica: Glaucoma
Categoria / Classificação: Pesquisa Básica
Região onde foi realizada a pesquisa: Sudeste

INSTITUIÇÃO ONDE FOI REALIZADO O TRABALHO:

CONEP:

AUTOR PRINCIPAL:

CO-AUTOR(ES):

TÍTULO:
EFFECTS OF ROSMARINIC ACID IN SUPRESSING RESPONSES CONTRIBUTING TO FIBROSIS IN TGF-BETA-STIMULATED TENON'S FIBROBLASTS

OBJETIVO:
Myofibroblast differentiation is related to collagen deposition, which is a key factor related to subconjunctival scarring observed after glaucoma filtration surgery. We have previously described that Rosmarinic acid (RA), an herbal polyphenol, decreases myofibroblast differentiation in rabbit Tenon’s capsule fibroblasts (RTF). We now evaluated if RA also suppresses fibrosis factors in transforming growth factor (TGF-beta-2) stimulated RTF.

MÉTODO:
Fibroblasts obtained from New Zealand rabbits were cultured in Dulbecco's modified Eagle's medium (DMEM). At the third passage, RTF was incubated with recombinant TGF-beta2 5ng/ml for 48 h, before being treated with RA. The dose dependent effects of AR (i.e. 0.3, 1.0 and 3.0 μM) were determined in triplicate after 24 h with the MTT assay. Real-time reverse transcription polymerase chain reaction evaluated type I alpha I collagen (COL1A1) and TGF-beta2 gene expression.

RESULTADOS:
RTF proliferation was raised by TGF-beta2 stimulation at 24h (p<0,05). AR induced declines in RTF proliferation, in the absence of TGF-beta2, only at the dose 3.0 μM (p=0.0062). However, there is no inhibition effect of RA on rises in proliferation induced by TGF-beta2. TGF-beta2 incubation also induced increases in COL1A1 expression (p=0.021). Although all RA concentrations suppressed COL1A1 mRNA in the absence of TGF-beta-2, they did not decrease significantly COL1A1 expression after TGF-beta2 exposure.

CONCLUSÕES:
TGF-beta2 stimulation reduced declines in RTF proliferation observed with AR treatment. Although AR decreased COL1A1 gene expression in the absence of TGF-beta2, in the presence of TGF-beta2 AR had no effect on both this response and TGF-beta2 expression. The present work suggests that AR may not be effective in modulating TGF-beta2-stimulated RTF, but it may still be somewhat useful as an adjunctive agent.

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