OBJECTIVE: To investigate the effect of brain functional recovery decoction(BFRD) on expression of vascular endothelial growth factor(VEGF) and angiopoietin-1(Ang-1) protein in rats with cerebral ischemia reperfusion ...OBJECTIVE: To investigate the effect of brain functional recovery decoction(BFRD) on expression of vascular endothelial growth factor(VEGF) and angiopoietin-1(Ang-1) protein in rats with cerebral ischemia reperfusion injury, and to explore the mechanism of action of BFRD.METHODS: Using the suture-occlusion method, a Wistar rat model of focal cerebral ischemia reperfusion was established. The rats were randomly divided into treatment group, model group, and sham operation group. The treatment group was administered BFRD. In situ hybridization was used to detect VEGF m RNA expression. Immunohistochemistry was used to observe expression of Ang-1 protein.RESULTS: VEGF mRNA expression was greater in the model group compared with the sham operation group(P < 0.05); Ang-1 protein expression was more obvious in the treatment group than the model group(P < 0.05).CONCLUSION: BFRD promoted VEGF m RNA and Ang-1 protein expression in the brains of rats with cerebral ischemia, suggesting increased angiogenesis.展开更多
Mild traumatic brain injury（TBI）, also called concussion, initiates sequelae leading to motor deficits, cognitive impairments and subtly compromised neurobehaviors. While the acute phase of TBI is associated with ne...Mild traumatic brain injury（TBI）, also called concussion, initiates sequelae leading to motor deficits, cognitive impairments and subtly compromised neurobehaviors. While the acute phase of TBI is associated with neuroinflammation and nitroxidative burst, the chronic phase shows a lack of stimulation of the neurorepair process and regeneration. The deficiency of nitric oxide（NO）, the consequent disturbed NO metabolome, and imbalanced mechanisms of S-nitrosylation are implicated in blocking the mechanisms of neurorepair processes and functional recovery in the both phases. Hypoxia inducible factor-1 alpha（HIF-1α）, a master regulator of hypoxia/ischemia, stimulates the process of neurorepair and thus aids in functional recovery after brain trauma. The activity of HIF-1α is regulated by NO via the mechanism of S-nitrosylation of HIF-1α. S-nitrosylation is dynamically regulated by NO metabolites such as S-nitrosoglutathione（GSNO） and peroxynitrite. GSNO stabilizes, and peroxynitrite destabilizes HIF-1α. Exogenously administered GSNO was found not only to stabilize HIF-1α and to induce HIF-1α-dependent genes but also to stimulate the regeneration process and to aid in functional recovery in TBI animals.展开更多
基金International Cooperation Projects of Shaanxi Province(The Protection on Ischemia-reperfusion Rats and the influence of VEGF RNA Expression of Brain Functional Recovery Decoction,No.2012-Kw-33-02)
文摘OBJECTIVE: To investigate the effect of brain functional recovery decoction(BFRD) on expression of vascular endothelial growth factor(VEGF) and angiopoietin-1(Ang-1) protein in rats with cerebral ischemia reperfusion injury, and to explore the mechanism of action of BFRD.METHODS: Using the suture-occlusion method, a Wistar rat model of focal cerebral ischemia reperfusion was established. The rats were randomly divided into treatment group, model group, and sham operation group. The treatment group was administered BFRD. In situ hybridization was used to detect VEGF m RNA expression. Immunohistochemistry was used to observe expression of Ang-1 protein.RESULTS: VEGF mRNA expression was greater in the model group compared with the sham operation group(P < 0.05); Ang-1 protein expression was more obvious in the treatment group than the model group(P < 0.05).CONCLUSION: BFRD promoted VEGF m RNA and Ang-1 protein expression in the brains of rats with cerebral ischemia, suggesting increased angiogenesis.
基金supported by grants from VA merit awards(BX3401 and RX2090)
文摘Mild traumatic brain injury（TBI）, also called concussion, initiates sequelae leading to motor deficits, cognitive impairments and subtly compromised neurobehaviors. While the acute phase of TBI is associated with neuroinflammation and nitroxidative burst, the chronic phase shows a lack of stimulation of the neurorepair process and regeneration. The deficiency of nitric oxide（NO）, the consequent disturbed NO metabolome, and imbalanced mechanisms of S-nitrosylation are implicated in blocking the mechanisms of neurorepair processes and functional recovery in the both phases. Hypoxia inducible factor-1 alpha（HIF-1α）, a master regulator of hypoxia/ischemia, stimulates the process of neurorepair and thus aids in functional recovery after brain trauma. The activity of HIF-1α is regulated by NO via the mechanism of S-nitrosylation of HIF-1α. S-nitrosylation is dynamically regulated by NO metabolites such as S-nitrosoglutathione（GSNO） and peroxynitrite. GSNO stabilizes, and peroxynitrite destabilizes HIF-1α. Exogenously administered GSNO was found not only to stabilize HIF-1α and to induce HIF-1α-dependent genes but also to stimulate the regeneration process and to aid in functional recovery in TBI animals.
