Abstract
Background: The hallmarks of non-alcoholic steatohepatitis are inflammation, ongoing liver cell damage, and the accumulation of hepatic fat. Although the pathogenesis is not fully understood yet, there is clear evidence that disease progression is associated with an increased ratio of lysophosphatidylcholine (LPC) to phosphatidylcholine (PC), which is an indicator of elevated phospholipase A2 (PLA2) activity. The isoform iPLA2β is a member of the fatty acid uptake complex and has an intrinsic capability to generate LPC, while the bile acid phospholipid conjugate, ursodeoxycholate-lysophosphatidylethanolamide (UDCA-LPE) inhibits iPLA2β and suppresses pro-inflammatory LPC generation in a dose-dependent mode. However, the precise mode of activity of this inhibition is still enigmatic.
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