Ozbal Seda, Erbil Güven, Koçdor Hilal, Tuğyan Kazim, Pekçetin Cetin, Ozoğul Candan
Department of Histology and Embryology, School of Medicine, Dokuz Eylul University Inciralti, TR-35340, Izmir, Turkey.
Neurosci Lett. 2008 Jun 27;438(3):265-9. doi: 10.1016/j.neulet.2008.03.091. Epub 2008 Apr 4.
It is known that the brain tissue is extremely sensitive to ischemia-reperfusion (IR) injury and therefore, brain ischemia and consecutive reperfusion result in neural damage and apoptosis. The proinflammatory cytokines such as tumor necrosis factor alfa (TNF-alpha) and interleukin-1 beta (IL-1beta) are produced during neurological disorders including cerebral ischemia. On the other hand, nerve growth factor (NGF), which is essential for the differentiation, survival and functions of neuronal cells in the central nervous system, regulate neuronal development through cell survival and cell death signaling. In the present study, we aimed to investigate the effect of selenium (Se) on prefrontal cortex and hippocampal damage in rats subjected to cerebral IR injury. Selenium was injected intraperitoneally at the doses of 0.625 mg/(kg day) after induction of IR injury. Prefrontal cortex and hippocampal damage was examined by cresyl-violet staining. Apostain and caspase-3 immune staining were used to detect apoptosis. TNF-alpha, IL-1beta and NGF levels were also evaluated. Histopathological evaluation showed that treatment with selenium after ischemia significantly attenuated IR-induced neuronal death in prefrontal cortex and hippocampal CA1 regions of rats. Apoptotic cells stained with apostain and caspase-3 were significantly decreased in treatment group when compared with the IR group. Additionally, treatment with selenium decreased the TNF-alpha and IL-1beta levels and increased the NGF levels in prefrontal cortex and hippocampal tissue of animals subjected to IR. The present results suggest that selenium is potentially a beneficial agent in treating IR-induced brain injury in rats.
已知脑组织对缺血再灌注（IR）损伤极为敏感，因此，脑缺血及随后的再灌注会导致神经损伤和细胞凋亡。在包括脑缺血在内的神经疾病过程中会产生促炎细胞因子，如肿瘤坏死因子α（TNF-α）和白细胞介素-1β（IL-1β）。另一方面，神经生长因子（NGF）对中枢神经系统中神经元细胞的分化、存活及功能至关重要，它通过细胞存活和细胞死亡信号来调节神经元发育。在本研究中，我们旨在探讨硒（Se）对脑IR损伤大鼠前额叶皮质和海马损伤的影响。在诱导IR损伤后，以0.625毫克/（千克·天）的剂量腹腔注射硒。通过甲酚紫染色检查前额叶皮质和海马损伤情况。使用凋亡染色和半胱天冬酶-3免疫染色来检测细胞凋亡。还评估了TNF-α、IL-1β和NGF水平。组织病理学评估表明，缺血后用硒治疗可显著减轻IR诱导的大鼠前额叶皮质和海马CA1区神经元死亡。与IR组相比，治疗组中用凋亡染色和半胱天冬酶-3染色的凋亡细胞明显减少。此外，用硒治疗可降低IR处理动物前额叶皮质和海马组织中的TNF-α和IL-1β水平，并提高NGF水平。目前的结果表明，硒可能是治疗大鼠IR诱导脑损伤的有益药物。
