Sharma Pushpa, Benford Brandi, Li Zhao Z, Ling Geoffrey Sf
Department of Anesthesiology, Uniformed Services University of the Health Sciences, Bethesda MD 20814, USA.
J Emerg Trauma Shock. 2009 May;2(2):67-72. doi: 10.4103/0974-2700.50739.
The present study was designed to investigate the role of a mitochondrial enzyme pyruvate dehydrogenase (PDH) on the severity of brain injury, and the effects of pyruvate treatment in rats with traumatic brain injury (TBI).
We examined rats subjected to closed head injury using a fluid percussion device, and treated with sodium pyruvate (antioxidant and substrate for PDH enzyme). At 72 h post injury, blood was analyzed for blood gases, acid-base status, total PDH enzyme using a dipstick test and malondialdehyde (MDA) levels as a marker of oxidative stress. Brain homogenates from right hippocampus (injured area) were analyzed for PDH content, and immunostained hippocampus sections were used to determine the severity of gliosis and PDH E1-infinity subunit.
Our data demonstrate that TBI causes a significant reduction in PDH enzyme, disrupt-acid-base balance and increase oxidative stress in blood. Also, lower PDH enzyme in blood is related to the increased gliosis and loss of its PDH E1-infinity subunit PDH in brain tissue, and these effects of TBI were prevented by pyruvate treatment.
Lower PDH enzyme levels in blood are related to the global oxidative stress, increased gliosis in brain, and severity of brain injury following TBI. These effects can be prevented by pyruvate through the protection of PDH enzyme and its subunit E-1.
本研究旨在探讨线粒体酶丙酮酸脱氢酶（PDH）在脑损伤严重程度中的作用，以及丙酮酸治疗对创伤性脑损伤（TBI）大鼠的影响。
我们使用流体冲击装置对大鼠进行闭合性颅脑损伤，并给予丙酮酸钠（PDH酶的抗氧化剂和底物）治疗。在损伤后72小时，分析血液中的血气、酸碱状态，使用试纸法检测总PDH酶，并检测丙二醛（MDA）水平作为氧化应激的标志物。分析右侧海马（损伤区域）的脑匀浆中的PDH含量，并用免疫染色的海马切片来确定胶质增生的严重程度和PDH E1-无穷亚基。
我们的数据表明，TBI导致血液中PDH酶显著降低，破坏酸碱平衡并增加氧化应激。此外，血液中较低的PDH酶与脑组织中胶质增生增加及其PDH E1-无穷亚基PDH的丢失有关，而丙酮酸治疗可预防TBI的这些影响。
血液中较低的PDH酶水平与TBI后的全身氧化应激、脑内胶质增生增加以及脑损伤严重程度有关。丙酮酸可通过保护PDH酶及其E-1亚基来预防这些影响。
