Significance of Alteration of Phospholipase C-δ1 in the Brain Tissues through Oxidative Stress

高氧诱导大鼠大脑皮质氧化应激时，大脑皮层磷脂酶C-β-1和-δ-1的蛋白水平显著升高，而磷脂酶C-γ-1的蛋白水平无明显变化。这些结果表明，高氧对大脑皮层造成氧化应激，PLC-β1和-δ1的蛋白水平发生了变化，而PLC-γ1的蛋白水平没有变化。丙烯腈(CAN)似乎通过选择性地诱导大鼠脑内的氧化应激而诱发星形细胞瘤。高氧组大鼠心脏和大脑皮层发生脂质过氧化反应，且对后者的影响大于前者。在经CaN处理的大脑皮层中，胞浆中的PLC-β1和-δ1，胞液、颗粒组分和溶出物中的PLC-γ1显著增加。在未检测到PLC-β1的大鼠心脏中，高氧可使胞液和颗粒组分中的PLC-γ1和-δ1分别增加和减少。此外，处理还降低了裂解液中PLC-γ1的表达水平。在经CaN处理的心脏中，PLC-γ1的水平无明显变化，而PLC-δ1在各组分均升高。我们已经证明，在心脏作为外周组织和大脑皮层作为中枢组织中，高氧引起的氧化应激明显低于CaN引起的氧化应激。在两种形式的氧化应激下，PLC同工酶的蛋白质水平都发生了变化，但不同水平的氧化应激之间以及不同器官之间的变化蛋白水平存在明显差异。为了解PLC同工酶在中枢神经系统发育和衰老中的作用，采用免疫组织化学方法检测了大鼠脑内Caspase家族蛋白在发育和衰老过程中的表达及其在细胞内的分布。

When oxidative stress is induced in the rat cerebral cortex through hyperoxia, the protein levels of phospholipase C (PLC)-β1 and -δ1 were significantly increased in the cerebral cortex, although that of PLC-γ1 was not altered. These results suggest that hyperoxia exerts oxidative stress on the rat cerebral cortex, and the protein levels of PLC-β1 and -δ1, but not PLC-γ1, were changed. Acrylonitrile (CAN) appears to induce astrocytomas through induction of oxidative stress on the rat brain selectively. Treatment of rats with CAN, but not hyperoxia, resulted in lipid peroxidation in the heart and cerebral cortex, and the effect on the latter was greater than on the former. In the CAN-treated cerebral cortex, significant increases in the PLC-β1 and -δ1 in the cytosol, and PLC-γ1 in the cytosolic and particulate fractions, and lysate were observed. In the rat heart, in which PLC-β1 could not be detected, PLC-γ1 and -δ1 were increased and decreased in the cytosolic and particulate fractions, respectively, by hyperoxia. In addition, the expression level of PLC-γ1 was decreased in the lysate by the treatment. In the heart treated with CAN, there was no change in the level of PLC-γ1, while PLC-δ1 was elevated in all fractions. We have demonstrated that oxidative stress induced by hyperoxia is apparently less than that induced by CAN administration in the heart as a peripheral tissue and the cerebral cortex as a central one. With both forms of oxidative stress, the protein levels of PLC isozymes were altered, but there was apparent difference in the altered protein levels between the different levels of oxidative stress, and between the organs. In order to obtain the information about contribution of PLC isozymes to the central nervous system development and aging, the expression of rat brain caspase family proteins in development and aging, and their subcellular distribution were also assessed using immunochemical detection.