This study used a novel combination of in vivo and in vitro experiments to show that Braintone had neuroprotective effects and clarified the molecular mechanisms underlying its efficacy. The Chinese herbal extract Bra...This study used a novel combination of in vivo and in vitro experiments to show that Braintone had neuroprotective effects and clarified the molecular mechanisms underlying its efficacy. The Chinese herbal extract Braintone is composed of Radix Rhodiolase Essence, Radix Notoginseng Essence, Fofium Ginkgo Essence and Rhizoma Chuanxiong. In vivo experiments showed that cerebral infarction volume was reduced, hemispheric water content decreased, and neurological deficits were alleviated in a rat model of permanent middle cerebral artery occlusion after administration of 87.5, 175 or 350 mg/kg Braintone for 7 consecutive days. Western blot analysis showed that Braintone enhanced the expression of hypoxia-inducible factor la, heme oxygenase-1 and vascular endothe- lial growth factor in the ischemic cortex of these rats. The 350 mg/kg dose of Braintone produced the most dramatic effects. For the in vitro experiments, prior to oxygen-glucose deprivation, rats were intragastrically injected with 440, 880 or 1 760 mg/kg Braintone to prepare a Braintone-co ntaining serum, which was used to pre-treat human umbilical vein endothelial cells for 24 hours. Human umbilical vein endothelial cell injury was alleviated with this pre-treatment. Western blot and real-time PCR analysis showed that the Braintone-containing serum increased the levels of hy- poxia-inducible factor la mRNA and protein, heine oxygenase-1 protein and vascular endothelial growth factor mRNA in oxygen-glucose deprived human umbilical vein endothelial cells. The 1 760 mg/kg dose produced the greatest increases in expression. Collectively, these experimental findings suggest that Braintone has neuroprotective effects on ischemia-induced brain damage via the up-regulation of hypoxia-inducible factor la, heme oxygenase-1 and vascular endothelial growth factor expression in vascular endothelial cells.展开更多
Through investigating the effect of mild hypothermia on activity of nitric oxide snythase (NOS) in cortical neurons and glycemia levels of neonatal rats with hypoxic ischemic brain damage (HIBD). We studied the mecha...Through investigating the effect of mild hypothermia on activity of nitric oxide snythase (NOS) in cortical neurons and glycemia levels of neonatal rats with hypoxic ischemic brain damage (HIBD). We studied the mechanism of protecting hypoxic ischemic neurons of mild hypothermia. We established neonatal rat HIBD models, used NOS immunohistochemistry and glycemia determination by micromethod. The number of cortical NOS positive neurons after hypoxic ischemia was significantly decreased as compared with controls. The glycemia levels was significantly increased than that controls. No significant difference was found in number of cortical NOS positive neurons and glycemia levels between 31℃ and 34℃ mild hypothemia. The results imply that hypothermia can decrease overproduction of NO through inhibiting the increase of the activity of NOS, and increase the glycemia levels, thus protect the hypoxic ischemic neurons.展开更多
Objective: To investigate the role of endothelin 1 (ET 1) in development of ischemic brain damage after subarachnoid hemorrhage (SAH), and the protective effect of Ginkgo biloba extract (GBE) on it. Methods: Noncr...Objective: To investigate the role of endothelin 1 (ET 1) in development of ischemic brain damage after subarachnoid hemorrhage (SAH), and the protective effect of Ginkgo biloba extract (GBE) on it. Methods: Noncraniotomy SAH models of Wistar rat were divided into SAH group and GBE treated group, the diameter of basilar artery (BA), dynamic changes of regional cerebral blood flow (rCBF) and ET 1 content of intracranial plasma within 24 hours after SAH of both groups were determined. And pathological examination of CA1 region of hippocampus was performed 3 days later. Results: rCBF decreased and ET 1 content increased obviously and steadily in 24 hours after SAH. Spasm of BA occurred half an hour after SAH and neurons of hippocampus CA1 region were damaged severely. GBE could antagonize the above mentioned pathological changes effectively. Conclusion:Increase of ET 1 is an important factor leading to ischemic brain damage after SAH. GBE exerts its protective effect by antagonizing pathological increase of ET 1.展开更多
基金supported by grants from the National Natural Science Foundation of China, No.30973510Scientific Research Foundation for Returned Overseas Chinese Scholars, State Education Ministry, No. K513400110a project funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions
文摘This study used a novel combination of in vivo and in vitro experiments to show that Braintone had neuroprotective effects and clarified the molecular mechanisms underlying its efficacy. The Chinese herbal extract Braintone is composed of Radix Rhodiolase Essence, Radix Notoginseng Essence, Fofium Ginkgo Essence and Rhizoma Chuanxiong. In vivo experiments showed that cerebral infarction volume was reduced, hemispheric water content decreased, and neurological deficits were alleviated in a rat model of permanent middle cerebral artery occlusion after administration of 87.5, 175 or 350 mg/kg Braintone for 7 consecutive days. Western blot analysis showed that Braintone enhanced the expression of hypoxia-inducible factor la, heme oxygenase-1 and vascular endothe- lial growth factor in the ischemic cortex of these rats. The 350 mg/kg dose of Braintone produced the most dramatic effects. For the in vitro experiments, prior to oxygen-glucose deprivation, rats were intragastrically injected with 440, 880 or 1 760 mg/kg Braintone to prepare a Braintone-co ntaining serum, which was used to pre-treat human umbilical vein endothelial cells for 24 hours. Human umbilical vein endothelial cell injury was alleviated with this pre-treatment. Western blot and real-time PCR analysis showed that the Braintone-containing serum increased the levels of hy- poxia-inducible factor la mRNA and protein, heine oxygenase-1 protein and vascular endothelial growth factor mRNA in oxygen-glucose deprived human umbilical vein endothelial cells. The 1 760 mg/kg dose produced the greatest increases in expression. Collectively, these experimental findings suggest that Braintone has neuroprotective effects on ischemia-induced brain damage via the up-regulation of hypoxia-inducible factor la, heme oxygenase-1 and vascular endothelial growth factor expression in vascular endothelial cells.
文摘Through investigating the effect of mild hypothermia on activity of nitric oxide snythase (NOS) in cortical neurons and glycemia levels of neonatal rats with hypoxic ischemic brain damage (HIBD). We studied the mechanism of protecting hypoxic ischemic neurons of mild hypothermia. We established neonatal rat HIBD models, used NOS immunohistochemistry and glycemia determination by micromethod. The number of cortical NOS positive neurons after hypoxic ischemia was significantly decreased as compared with controls. The glycemia levels was significantly increased than that controls. No significant difference was found in number of cortical NOS positive neurons and glycemia levels between 31℃ and 34℃ mild hypothemia. The results imply that hypothermia can decrease overproduction of NO through inhibiting the increase of the activity of NOS, and increase the glycemia levels, thus protect the hypoxic ischemic neurons.
文摘Objective: To investigate the role of endothelin 1 (ET 1) in development of ischemic brain damage after subarachnoid hemorrhage (SAH), and the protective effect of Ginkgo biloba extract (GBE) on it. Methods: Noncraniotomy SAH models of Wistar rat were divided into SAH group and GBE treated group, the diameter of basilar artery (BA), dynamic changes of regional cerebral blood flow (rCBF) and ET 1 content of intracranial plasma within 24 hours after SAH of both groups were determined. And pathological examination of CA1 region of hippocampus was performed 3 days later. Results: rCBF decreased and ET 1 content increased obviously and steadily in 24 hours after SAH. Spasm of BA occurred half an hour after SAH and neurons of hippocampus CA1 region were damaged severely. GBE could antagonize the above mentioned pathological changes effectively. Conclusion:Increase of ET 1 is an important factor leading to ischemic brain damage after SAH. GBE exerts its protective effect by antagonizing pathological increase of ET 1.
