Cytoneurobiology Unit & Laboratory of Aging and Nervous Diseases, Medical College of Soochow University, Suzhou Industrial Park, Suzhou, Jiangsu 215123, People's Republic of China.
Mol Cell Biochem. 2010 Feb;335(1-2):127-36. doi: 10.1007/s11010-009-0249-4. Epub 2009 Sep 17.
Pancreatic triglyceride lipase (PTL), an enzyme of digestive system, plays very important roles in the digestion and absorption of lipids. However, its distribution and function in the central nervous system (CNS) remains unclear. In the present study, we mainly investigated the expression and cellular localization of PTL during traumatic brain injury (TBI). Western blot and RT-PCR analysis revealed that PTL was present in normal rat brain cortex. It gradually increased, 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 colocalizations in astrocytes. When TBI occurred in the rat cortex, the expression of PTL gradually increased, reached the peak at the 3rd day after TBI, and then decreased. Importantly, more PTL was colocalized with astrocytes, which is positive for proliferating cell nuclear antigen (PCNA). In addition, Western blot detection showed that the 3rd day post injury was not only the proliferation peak indicated by the elevated expression of PCNA, glial fibrillary acidic protein (GFAP) and cyclin D1, but also the apoptotic peak implied by the alteration of caspase-3 and bcl-2. These data suggested that PTL may be involved in the pathophysiology of TBI and PTL may be complicated after injury, more PTL was colocalized with astrocytes. Importantly, injury-induced expression of PTL was colabelled by proliferating cell nuclear antigen (proliferating cells marker), and the western blot for GFAP, PCNA and cyclin D1, showed that 3 days post injury was the proliferation peak, in coincidence to it, the protein level change of caspase-3 and bcl-2 revealed that the stage was peak of apoptotic too. These data suggested that PTL may be involved in the pathophysiology of TBI and that PTL may be implicated in the proliferation of astrocytes and the recovery of neurological outcomes. But the inherent mechanisms remained unknown. Further studies are needed to confirm the exact role of PTL after brain injury.
胰腺甘油三酯脂肪酶（PTL）是一种消化系统酶，在脂质的消化和吸收中发挥着非常重要的作用。然而，其在中枢神经系统（CNS）中的分布和功能尚不清楚。在本研究中，我们主要研究了创伤性脑损伤（TBI）过程中 PTL 的表达和细胞定位。Western blot 和 RT-PCR 分析显示 PTL 存在于正常大鼠大脑皮质中。它逐渐增加，在 TBI 后第 3 天达到峰值，然后下降。双重免疫荧光染色显示 PTL 与神经元共表达，但与星形胶质细胞的共定位较少。当大鼠皮质发生 TBI 时，PTL 的表达逐渐增加，在 TBI 后第 3 天达到峰值，然后下降。重要的是，更多的 PTL 与星形胶质细胞共定位，这些星形胶质细胞呈增殖细胞核抗原（PCNA）阳性。此外，Western blot 检测显示，损伤后第 3 天不仅是 PCNA、胶质纤维酸性蛋白（GFAP）和细胞周期蛋白 D1 表达升高所表示的增殖高峰，也是 caspase-3 和 bcl-2 改变所暗示的凋亡高峰。这些数据表明 PTL 可能参与 TBI 的病理生理学过程，PTL 可能在损伤后变得复杂，更多的 PTL 与星形胶质细胞共定位。重要的是，损伤诱导的 PTL 表达与增殖细胞核抗原（增殖细胞标志物）共定位，GFAP、PCNA 和细胞周期蛋白 D1 的 Western blot 显示，损伤后第 3 天是增殖高峰，与之巧合的是，caspase-3 和 bcl-2 的蛋白水平变化表明该阶段也是凋亡高峰。这些数据表明 PTL 可能参与 TBI 的病理生理学过程，并且 PTL 可能涉及星形胶质细胞的增殖和神经功能恢复。但内在机制尚不清楚。需要进一步的研究来确认脑损伤后 PTL 的确切作用。
