trans-sodium-crocetinate has been researched along with Infarction--Middle-Cerebral-Artery* in 2 studies
2 other study(ies) available for trans-sodium-crocetinate and Infarction--Middle-Cerebral-Artery
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Metabolic reflow as a therapy for ischemic brain injury.
Ischemic neuronal damage is a common feature of occlusive strokes, hemorrhagic strokes, and traumatic brain injury. In addition, ischemia can be an anticipated or unanticipated complication of a variety of surgical procedures. Most therapeutic strategies for managing ischemic injury seek to re-establish blood flow, suppress neural metabolism, and/or limit specific cellular injury cascades. An alternative therapeutic approach is to enhance the delivery of metabolic substrates to ischemic tissue. This strategy is typified by efforts to increase tissue oxygenation by elevating the levels of circulating oxygen. Our studies are examining a complementary approach in which the delivery of metabolic substrates is enhanced by facilitating the diffusion of oxygen and glucose from the vasculature into neural tissue during ischemia. This is achieved by increasing the diffusivity of small molecules in aqueous solutions, such as plasma and interstitial fluid. The carotenoid compound, trans-sodium crocetinate (TSC) is capable of increasing oxygen and glucose diffusivity, and our studies demonstrate that TSC increases cerebral tissue oxygenation in the penumbra of a focal ischemic event. In addition, TSC treatment reduces the volume of cerebral infarction in rodent models of both permanent and temporary focal ischemia. This strategy of "metabolic reflow" thus blunts the metabolic challenge in partially-perfused tissue and reduces ischemic neural injury. Topics: Animals; Carotenoids; Cerebral Infarction; Cerebrovascular Circulation; Disease Models, Animal; Glucose; Infarction, Middle Cerebral Artery; Male; Oxygen; Oxygen Consumption; Rats; Rats, Sprague-Dawley; Time Factors; Vitamin A | 2011 |
Protective effects of carotenoids from saffron on neuronal injury in vitro and in vivo.
Crocus sativus L. (saffron) has been used as a spice for flavoring and coloring food preparations, and in Chinese traditional medicine as an anodyne or tranquilizer. Our previous study demonstrated that crocin, a carotenoid pigment of saffron, can suppress the serum deprivation-induced death of PC12 cells by increasing glutathione (GSH) synthesis and thus inhibiting neutral sphingomyelinase (nSMase) activity and ceramide formation. The carotenoid pigments of saffron consist of crocetin di-(beta-d-glucosyl)-ester [dicrocin], crocetin-(beta-d-gentiobiosyl)-(beta-d-glucosyl)-ester [tricrocin] and crocetin-di-(beta-d-gentiobiosyl)-ester [crocin]. Saffron also contains picrocrocin, the substance causing saffron's bitter taste. In this study, to confirm whether neuroprotective effects of saffron are caused solely by crocin, we examined the antioxidant and GSH-synthetic activities of these crocins in PC12 cells under serum-free and hypoxic conditions. Measurements of cell viability, peroxidized membrane lipids and caspase-3 activity showed that the rank order of the neuroprotective potency at a concentration of 10 muM was crocin>tricrocin>dicrocin and picrocrocin (the latter two crocins had a little or no potency). In addition, we show that among these saffron's constituents, crocin most effectively promotes mRNA expression of gamma-glutamylcysteinyl synthase (gamma-GCS), which contributes to GSH synthesis as the rate-limiting enzyme, and that the carotenoid can significantly reduce infarcted areas caused by occlusion of the middle cerebral artery (MCA) in mice. Topics: Animals; Antioxidants; Brain Infarction; Carotenoids; Caspase 3; Cell Hypoxia; Cell Survival; Crocus; Cyclohexenes; Disease Models, Animal; Glucosides; Glutamate-Cysteine Ligase; Glutathione; Infarction, Middle Cerebral Artery; Lipid Peroxidation; Male; Membrane Lipids; Mice; Molecular Structure; Neurons; Neuroprotective Agents; PC12 Cells; Rats; Structure-Activity Relationship; Terpenes; Time Factors; Vitamin A | 2007 |