Aims: 

Our previous investigations have established that phosphatidylcholine (PC) inhibits the production of reactive oxygen species (ROS) both in vitro and in vivo, and displays an anti-inflammatory effectiveness proportional to the amount of methane generation and the number of methyl groups in the compounds (Cell Physiol Biochem 2008, Shock 2008). Our present aims were to examine whether the anti-inflammatory effects of PC are linked to the fatty acid parts or to the headgroup, hence we repeated the crucial experiments with L-a glycerylphosphorylcholine (GPC), the deacilated polar derivative of PC, on the inflammatory consequences of ischaemia-reperfusion (IR).

Methods: 

Anesthetized rats were divided to control (n=8), mesenteric IR (n=8), IR with GPC pre-treatment (n=8) or IR with GPC post-treatment (n=8) groups. Macrohaemodynamic parameters (mean arterial pressure, superior mesenteric artery flow, mesenteric vascular resistance (MVR)) and microhaemodynamic parameters (intravital OPS videomicroscopy) were measured. Biochemical markers (tissue superoxide (O₂^.-), xanthine oxidoreductase (XOR) activity, and liver ATP-contents were also determined after 45 min ischemia and 180 min reperfusion period.

Results: 

Mesenteric IR increased the MVR and tissue O₂^.- production, and reduced liver ATP content. GPC pre-treatment alleviated the elevation of MVR and decreased the tissue O₂^.- production, while post-treatment decreased both XOR activity and ATP depletion, and normalized the intestinal microcirculatory dysfunction.

Conclusion: 

Exogenous GPC has anti-inflammatory attribute and decreases IR-induced ROS production. The similar efficacy of PC is linked to the polar part of the PC molecule.

Support: 

OTKA K75161; TÁMOP-4.2.1; TÁMOP-4.2.2; ETT 442/2009