Wang Chaoyun, Zhang Dalei, Li Guisheng, Liu Juntian, Tian Jingwei, Fu Fenghua, Liu Ke
Department of Pharmacology, Xi'an Jiaotong University School of Medicine, Xi'an, Shaanxi 710061, People's Republic of China.
Exp Brain Res. 2007 Mar;177(4):533-9. doi: 10.1007/s00221-006-0705-2. Epub 2006 Sep 28.
The present study was conducted to investigate whether safflor yellow B (SYB) had a protective effect on cerebral ischemic injury and to determine the possible mechanisms in vivo and in vitro. In vivo, Male Wistar-Kyoto (WKY) rats were used to make the model of middle cerebral artery occlusion (MCAO). The behavioral test was used to measure neurological deficit scores for evaluation of the ischemic damage of brain. The infarction area of brain was assessed in brain slices stained with 2% solution of 2,3,5-triphenyl tetrazolium chloride (TTC). Spectrophotometric assay was used to determine the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx), contents of malondialdehyde (MDA) and adenosine triphosphate (ATP) of the brain. Furthermore, the respiratory control ratio (RCR = state 3/state 4) was assessed in the brain mitochondria. In vitro, the effect of SYB was tested in cultured fetal cortical cells exposed to glutamate to identify its neuroprotection against neurons damage. The results in vivo showed that SYB at doses of 3.0 and 6.0 mg kg(-1) markedly decreased the neurological deficit scores and the infarction area in MCAO rats. At the same time, SYB significantly improved mitochondrial energy metabolism, decreased MDA content, and increased SOD and GPx activities in ischemic brain. The results in vitro showed that SYB remarkably inhibited neuron damage induced by glutamate in cultured fetal cortical cells. These suggest that SYB might act as a potential neuroprotective agent against the cerebral ischemia-induced injury in rat brain through reducing lipid peroxides, scavenging free radicals, and improving the energy metabolism.
本研究旨在探讨红花黄色素B(SYB)对脑缺血损伤是否具有保护作用,并确定其体内和体外的可能作用机制。在体内实验中,采用雄性Wistar-Kyoto(WKY)大鼠制作大脑中动脉闭塞(MCAO)模型。通过行为测试来测量神经功能缺损评分,以评估脑缺血损伤情况。用2%的2,3,5-三苯基氯化四氮唑(TTC)溶液对脑切片进行染色,评估脑梗死面积。采用分光光度法测定脑中超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPx)的活性、丙二醛(MDA)和三磷酸腺苷(ATP)的含量。此外,还评估了脑线粒体中的呼吸控制率(RCR = 状态3/状态4)。在体外实验中,在暴露于谷氨酸的培养胎鼠皮质细胞中测试SYB的作用,以确定其对神经元损伤的神经保护作用。体内实验结果表明,3.0和6.0 mg kg(-1)剂量的SYB显著降低了MCAO大鼠的神经功能缺损评分和梗死面积。同时,SYB显著改善了缺血脑线粒体的能量代谢,降低了MDA含量,并提高了SOD和GPx的活性。体外实验结果表明,SYB显著抑制了培养胎鼠皮质细胞中谷氨酸诱导的神经元损伤。这些结果表明,SYB可能通过减少脂质过氧化、清除自由基和改善能量代谢,作为一种潜在的神经保护剂,对抗大鼠脑缺血诱导的损伤。