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The Neuroprotective Effects of Coccomyxa Gloeobotrydiformis on the Ischemic Stroke in a Rat Model

机译:球孢球菌对大鼠缺血性中风的神经保护作用

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摘要

Stroke is a major cause of mortality and the leading cause of permanent disability. In this study, we adopted the classic middle cerebral artery occlusion(MCAO) stroke model to observe the therapeutic effects of coccomyxa gloeobotrydiformis(CGD) on ischemic stroke, and discuss the underlying mechanisms. Low dose (50 mg/kg.day) and high dose (100 mg/kg.day) concentrations of the drug CGD were intragastrically administrated separately for 8 weeks. Infarct volumes, neurologic deficits and degree of stroke-induced brain edema were measured 24 hours after reperfusion. Furthermore, oxidative stress related factors (SOD and MDA), mitochondrial membrane potential, and apoptosis regulatory factors (mitochondrial Cyt-C, Bcl-2, Bax, and caspase-3) were all investigated in this research. We found that CGD attenuated cerebral infarction, brain edema and neurologic deficits; CGD maintained the mitochondrial membrane potential and decreased mitochondrial swelling. It also prevented oxidative damage by reducing MDA and increasing SOD. In addition, CGD could effectively attenuate apoptosis by restoring the level of mitochondrial Cyt C and regulating the expression of Bcl-2, Bax and caspase 3. These results revealed that CGD has a therapeutic effect on ischemic stroke, possibly by inducing mitochondrial protection and anti-apoptotic mechanisms.
机译:中风是死亡的主要原因,也是永久性残疾的主要原因。在这项研究中,我们采用经典的大脑中动脉闭塞(MCAO)中风模型来观察球果双球菌(CGD)对缺血性中风的治疗作用,并探讨其潜在机制。将低剂量(50 mg / kg.day)和高剂量(100 mg / kg.day)浓度的药物CGD分别在胃内给药8周。再灌注后24小时测量梗死体积,神经功能缺损和中风诱发的脑水肿程度。此外,本研究还研究了氧化应激相关因子(SOD和MDA),线粒体膜电位和凋亡调控因子(线粒体Cyt-C,Bcl-2,Bax和caspase-3)。我们发现,CGD可减轻脑梗死,脑水肿和神经功能缺损。 CGD保持线粒体膜电位并降低线粒体肿胀。它还通过降低MDA和增加SOD来防止氧化损伤。此外,CGD可以通过恢复线粒体Cyt C的水平并调节Bcl-2,Bax和caspase 3的表达来有效地减轻细胞凋亡。这些结果表明,CGD可能通过诱导线粒体保护和抗凋亡来治疗缺血性中风。 -凋亡机制。

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