Expression Of Pancreatic Triglyceride Lipase In Rat Traumatic Brain Injury And Cultured Astrocytes

Pancreatic triglyceride lipase (PTL), is a member of lipase family, plays very important roles in the digestion and absorption of lipids. Lipid is key composition of myelin sheath in nervous system and during the recent years, more and more people paid attention to investigate the role of lipid metabolism in formation of myelin sheath and regeneration and recovery of nervous after injury. It was reported that other members of lipase family, such as Lipoproten lipase (LPL) and Endothelial lipase (EL), involved in the formation of myelin sheath and nervous regeneration and functional recovery. Does the expression of PTL change during the central nervous system (CNS) injury and in the vitro cultured astrocytes? What kind of function of PTL in the injury of CNS? It was remained unreported.Objective Establish a traumatic brain injury model and explore the expression of PTL on the function of CNS injury and regeneration. Stimulate cultured astrocytes with different concentration of bacteria endotoxin LPS, to investigate the expression change of PTL, and further detect the role of PTL in astrocytes.Methods TBI model was induced in rat by using a microknife to form a unilateral controlled cortical injury. Western blot and RT-PCR were employed to detect PTL expression at different survival time and distribution after TBI. We used double immunofluorescence to dectect the cellular location of PTL and the marker molecular (PCNA, caspase-3) during TBI. And we also used Western blot to investigate the expression of GFAP, cyclinD1, PCNA, bcl-2 and caspase-3. We employed Western blot and double immunofluorescence to detect the change of PTL expression after astrocytes were stimulated by different concentration gradient of LPS.Results The RT-PCR and Western blot results revealed that the expression of PTL was increased after TBI, and reached a peak at the 3rd day after TBI, and then decreased. Double immunofluorescence staining showed that PTL was co-expressed with neuron, but had a few co-localizations in astrocytes. When TBI occurred in rat cortex, more PTL was colocalized with astrocytes, which was positive for proliferationg cell nuclear antigen (PCNA). In addition, Western blot detection showed that the 3rd day post injury was not only the proliferation of peak indicated by the elevated expression of PCNA, GFAP and cyclinD1, but also the apoptotic peak implied by the alteration of caspase-3 and bcl-2. After the astrocytes were stimulated by different concentration of LPS, the expression of PTL was increased, and it was increased in the cytoplasm and decreased in the nucleus.Conclusion PTL might be involved in the formation of myelin sheath and the neuro-degeneration and recovery of TBI and that PTL may be implicated in the proliferation of astrocytes and the recovery of neurological outcomes. The expression level and sub-cellular location of PTL were changed after stimulated by different concentration of LPS, so we proposed that PTL might be involved in the inflammation of astrocytes. But the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of PTL and the potential mechanisms after brain injury.