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Abstract
Introduction: We have shown that UDCA-LPE elicits protection by activating survival signalling pathways, and inhibits TNFα-induced apoptosis in vitro and inflammation in vivo when intraperitoneally (i.p) injected to galactosamine/endotoxin-treated mice. UDCA and phosphatidylcholine (PC) are known hepatoprotectants via membrane stabilization. We tested herein whether UDCA-LPE undergoes hydrolysis to UDCA and LPE, and whether it increases cellular UDCA, PC and other cytoprotective lipids. Methods: UDCA-LPE was used to treat mouse hepatocytes at 40–60µM or i.p injected to mice at 30mg/kg. Fatty acid analyses were performed using GC/MS. UDCA-LPE, UDCA, LPE, tauro-UDCA, glyco-UDCA, diacyl PC and lysoPC were analyzed by LC/MS. TaqMan RT-PCR was used for gene quantification. Results: Following UDCA-LPE administration, concentrations of UDCA and LPE were increased with a lag-time after UDCA-LPE in mouse hepatocytes as well as in plasma, urine, liver, and intestine. UDCA-LPE after i.p. was found in the liver maximizing after 4h and completely decayed after 8h. Following UDCA-LPE administration, diacyl PC and lyso PC levels were increased and kept sustained in plasma and liver even after 24h. Among PC synthesis genes measured, we found that UDCA-LPE upregulated CDP-diacylglycerol synthase–1 mRNA expression. In UDCA-LPE-treated mouse hepatocytes, tauro-UDCA, glyco-UDCA concentrations were also increased. During protection against lipoapoptosis by UDCA-LPE, the levels of medium-chain saturated fatty acids and plasmalogen dimethyl acetal 16: 1 were found to be increased. Plasmalogen is shown to be decreased with old age and NASH. Conclusions: UDCA-LPE increased cytoprotective conjugated-UDCA and PC species. UDCA-LPE protected against lipoapoptosis by increasing contents of plasmalogen 16: 1 and medium-chain saturated fatty acids. The latter is shown protective against NASH. UDCA-LPE can elicit protection against NASH by increasing contents of various hepatoprotective lipids.
Published Version
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