OBJECTIVE: To investigate the protective effect of neuroprotection against transient focal cerebral ischemia of the extract from Tianma(Rhizoma Gastrodiae) and the possible mechanisms underlying the action.METHODS: Ce...OBJECTIVE: To investigate the protective effect of neuroprotection against transient focal cerebral ischemia of the extract from Tianma(Rhizoma Gastrodiae) and the possible mechanisms underlying the action.METHODS: Cerebral ischemia-reperfusion injury was induced through middle cerebral artery occlusion(MCAO). Adult male Sprague-Dawley rats were randomly divided into four groups: sham-operated,ischemia-reperfusion model, 102.6 mg/kg extract treated and 11.4 mg/kg extract treated groups. The extract was prepared from gastrodia elata with ethyl acetate. The effect of the extract tested on rat neurological de fi cits and Cerebral index, cerebral infarct volume, brain injury, terminal dexynucleotidyl transferase-mediated d UTP nick end labeling(TUNEL) and B-cell lymphoma-2(Bcl-2) positive cells.RESULTS: The extract was able to reduce neurological scores, cerebral index and cerebral infarction rate. The brain injury was also relieved by the extract. The results of immunofluorescence staining analysis indicated that the extract increased the expression of Bcl-2 and reduced TUNEL-positive cells significantly in the extract treated groups.CONCLUSION: These results suggested that the extract relieved ischemic injury induced by transient focal cerebral ischemia in rats, and this neuroprotective effect might be partially due to the attenuated apoptosis pathway.展开更多
There are currently no federally approved neuroprotective agents to treat traumatic brain injury. Progesterone, a hydrophobic steroid hormone, has been shown in recent studies to exhibit neu-roprotective effects in co...There are currently no federally approved neuroprotective agents to treat traumatic brain injury. Progesterone, a hydrophobic steroid hormone, has been shown in recent studies to exhibit neu-roprotective effects in controlled cortical impact rat models. Akt is a protein kinase known to play a role in cell signaling pathways that reduce edema, inlfammation, apoptosis, and promote cell growth in the brain. This study aims to determine if progesterone modulates the phosphor-ylation of Aktvia its threonine 308 phosphorylation site. Phosphorylation at the threonine 308 site is one of several sites responsible for activating Akt and enabling the protein kinase to carry out its neuroprotective effects. To assess the effects of progesterone on Akt phosphorylation, C57BL/6 mice were treated with progesterone （8 mg/kg） at 1 （intraperitonally）, 6, 24, and 48 hours （subcutaneously） post closed-skull traumatic brain injury. The hippocampus was harvest-ed at 72 hours post injury and prepared for western blot analysis. Traumatic brain injury caused a signiifcant decrease in Akt phosphorylation compared to sham operation. However, mice treat-ed with progesterone following traumatic brain injury had an increase in phosphorylation of Akt compared to traumatic brain injury vehicle. Our ifndings suggest that progesterone is a viable treatment option for activating neuroprotective pathways after traumatic brain injury.展开更多
基金Supported by Natural Science Foundation of China (Anti-ischemic Brain Injury and Neuroprotection Mechanisms of Phenolic Compounds Distributed in Brain from Gastrodia,No.81160514)Yunnan Applied Basic Research Projects (Protective Effect and Mechanisms of 4-Methoxybenzyl from Gastrodia Elata on the Neurovascular Unit,No.2014FB153)Traditional Chinese Medicine Education Innovation Fund of Yunnan Baiyao-Yunnan University of TCM (The Regulation Role of Ethyl Acetate Extract from Gastrodia Elata on NO Pathway,No.YB2014J04)
文摘OBJECTIVE: To investigate the protective effect of neuroprotection against transient focal cerebral ischemia of the extract from Tianma(Rhizoma Gastrodiae) and the possible mechanisms underlying the action.METHODS: Cerebral ischemia-reperfusion injury was induced through middle cerebral artery occlusion(MCAO). Adult male Sprague-Dawley rats were randomly divided into four groups: sham-operated,ischemia-reperfusion model, 102.6 mg/kg extract treated and 11.4 mg/kg extract treated groups. The extract was prepared from gastrodia elata with ethyl acetate. The effect of the extract tested on rat neurological de fi cits and Cerebral index, cerebral infarct volume, brain injury, terminal dexynucleotidyl transferase-mediated d UTP nick end labeling(TUNEL) and B-cell lymphoma-2(Bcl-2) positive cells.RESULTS: The extract was able to reduce neurological scores, cerebral index and cerebral infarction rate. The brain injury was also relieved by the extract. The results of immunofluorescence staining analysis indicated that the extract increased the expression of Bcl-2 and reduced TUNEL-positive cells significantly in the extract treated groups.CONCLUSION: These results suggested that the extract relieved ischemic injury induced by transient focal cerebral ischemia in rats, and this neuroprotective effect might be partially due to the attenuated apoptosis pathway.
文摘There are currently no federally approved neuroprotective agents to treat traumatic brain injury. Progesterone, a hydrophobic steroid hormone, has been shown in recent studies to exhibit neu-roprotective effects in controlled cortical impact rat models. Akt is a protein kinase known to play a role in cell signaling pathways that reduce edema, inlfammation, apoptosis, and promote cell growth in the brain. This study aims to determine if progesterone modulates the phosphor-ylation of Aktvia its threonine 308 phosphorylation site. Phosphorylation at the threonine 308 site is one of several sites responsible for activating Akt and enabling the protein kinase to carry out its neuroprotective effects. To assess the effects of progesterone on Akt phosphorylation, C57BL/6 mice were treated with progesterone （8 mg/kg） at 1 （intraperitonally）, 6, 24, and 48 hours （subcutaneously） post closed-skull traumatic brain injury. The hippocampus was harvest-ed at 72 hours post injury and prepared for western blot analysis. Traumatic brain injury caused a signiifcant decrease in Akt phosphorylation compared to sham operation. However, mice treat-ed with progesterone following traumatic brain injury had an increase in phosphorylation of Akt compared to traumatic brain injury vehicle. Our ifndings suggest that progesterone is a viable treatment option for activating neuroprotective pathways after traumatic brain injury.
