Evidence for a therapeutic effect of Braintone on ischemic brain damage***

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Abstract

Research Highlights

(1) The link between Braintone and pro-apoptotic genes (AT2 receptor, Fas, Bax and Bcl-XS) has been previously described by Kok-Poh Loh, Wan-Hui Wong and Li-Shan Low from the Department of Pharmacology, National University of Singapore in “Mechanisms of cerebral protection of Chinese herbal extract-Braintone on middle cerebral artery occluded rats”.

Research Highlights

(2) This study combined novel in vivo and in vitro experiments to show that Braintone dose- dependently increased the expression of hypoxia inducible factor 1α, heme oxygenase-1 and vascular endothelial growth factor in the ischemic cortex of rats with middle cerebral artery occlusion. The Chinese herbal extract Braintone is composed of Radix Rhodiolase Essence, Radix Notoginseng Essence, Folium Ginkgo Essence and Rhizoma Chuanxiong. Braintone-containing serum increased levels of hypoxia-inducible factor 1α mRNA and protein, and elevated vascular endothelial growth factor mRNA and heme oxygenase-1 protein expression in a dose-dependent manner in human umbilical vein endothelial cells after glucose-oxygen deprivation.

Research Highlights

(3) Braintone has a neuroprotective effect, which is mediated by the up-regulation of hypoxia inducible factor 1α, heme oxygenase-1 and vascular endothelial growth factor expression.

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, Folium 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 1α, heme oxygenase-1 and vascular endothelial 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-containing 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 hypoxia-inducible factor 1α mRNA and protein, heme 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 1α, heme oxygenase-1 and vascular endothelial growth factor expression in vascular endothelial cells.

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