科研之友
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摘要
Purpose: To investigate the effect of prostaglandin F2 alpha (PGF2 alpha), latanoprost, travoprost, bimatoprost, and tafluprost on human orbital preadipocyte differentiation and intracellular lipid storage, and to reveal the potential mechanisms by which topical prostaglandin analogs induce orbital fat volume reduction and cause deep superior sulcus syndrome. %26lt;br%26gt;Methods: Human orbital adipose precursors were treated in vitro for 24 h (day 1) with PGF2 alpha, latanoprost, travoprost, bimatoprost, and tafluprost in their commercial formulations (1:100 dilution). Expressions of adipogenic transcription factor, peroxisome proliferator-activated receptor-gamma (PPAR gamma), and CCAAT-enhancer-binding protein alpha (C/EBP alpha) were determined by real-time reverse transcription-polymerase chain reaction (RT-PCR) at day 7. At 14 days, cells were stained with oil red O, intracellular lipid accumulation was evaluated by lipid absorbance, and adipocyte expression marker [Lipoprotein lipase (LPL)] was determined by real-time RT-PCR. %26lt;br%26gt;Results: Our results showed that PGF2 alpha and topical prostaglandin analogs down-regulated the expression of PPAR gamma and C/EBP alpha, and inhibited accumulation of intra-cytoplasmic lipid droplets and expression of LPL compared with the untreated control. Comparison between the 4 drugs showed that latanoprost had the weakest antiadipogenic effect, and bimatoprost induced the most significant reduction of adipogenesis. %26lt;br%26gt;Conclusion: Latanoprost, travoprost, bimatoprost, and tafluprost inhibited human preadipocyte differentiation and intracellular lipid accumulation. Morphologic and metabolic changes in orbital adipocytes caused by PGF2 alpha analogs are a possible pathophysiologic explanation of superior eyelid deepening in patients with glaucoma.
- 出版日期2012-4
