Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0917798 (cerebral ischemia)
 17,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of this study was to explore the mechanism of 3-methoxy puerarin on decreasing the cerebral ischemia-reperfusion injury in rats. Before the model of cerebral ischemia-reperfusion injury was made, the rats in one group (3-methoxy puerarin group, 3-MP group) were pretreated with 3-methoxy puerarin (100 mg/kg) by gavageing two times per day for seven days. At an hour before operation, the rats in the 3-MP group were additionally given 3-methoxy puerarin by gavageing once. The level of prostacyclin (PGI2) and the expression of endothelin-1 (ET-1) mRNA in cerebral tissue, the activity of plasma tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor (PAI) were measured. Cerebral tissue pathologic changes were also observed. The levels of PGI2 in cerebral tissue and the activity of plasma t-PA in 3-MP group were significantly higher than those in the group of cerebral ischemia-reperfusion injury (CIRI group) (p<0.01). The activity of plasma PAI and the expression of ET-1 mRNA in cerebral tissue in 3-MP group were significantly lower than those in CIRI group (p<0.01). The cerebral tissue pathologic changes were significant in CIRI group, which were significantly ameliorated in the 3-MP group. The study showed, in the rat model of cerebral ischemia-reperfusion injury, 3-methoxy puerarin can not only increase the level of PGI2 in cerebral tissue and the activity of plasma t-PA, but also inhibit the activity of plasma PAI and the expression of ET-1 mRNA in cerebral tissue. Those findings might be the mechanisms behind the protecting effects of 3-methoxy puerarin on the cerebral ischemia-reperfusion injury.
Asia Pac J Clin Nutr 2007
PMID:The mechanism of 3-methoxy puerarin on decreasing the cerebral ischemia-reperfusion injury in rats. 1739 23

The aim of this study was to explore the effect of gastrodin on the level of amino acids in the striatum in the rats of cerebral ischemia-reperfusion injury. 30 male SD rats were randomly divided into 3 groups: the group of pseudo-operation (normal control group, NC group), the group of cerebral ischemia-reperfusion injury (CIRI group), and the group of cerebral ischemia-reperfusion injury treated with gastrodin (G group). Cerebral ischemia-reperfusion injury was induced through middle cerebral artery occlusion (MCAO). 10 minutes before the operation, the rats in the G group were injected with gastrodin (50 mg/kg) intraperitoneally once. The rats in the CIRI and NC group were injected with the same volume of 10% propylene glycol normal saline intraperitoneally once. The levels of glutamic acid (Glu), aspartic acid (Asp), gamma-aminobutyric acid (GABA), taurine (Tau) in striatum in the rats of the 3 groups were measured with the method of microdialysis-HPLC techniques. The ratio of Glu to GABA was calculated. The volume of cerebral infarction was quantified. This study showed that gastrodin can decrease the volume of cerebral infarction, ameliorate the cerebral injury in the rats of cerebral ischemia-reperfusion. The mechanisms might be that gastrodin can improve the level of amino acids in striatum.
Asia Pac J Clin Nutr 2007
PMID:Effects of gastrodin on amino acids after cerebral ischemia-reperfusion injury in rat striatum. 1739 24

Dipeptidyl peptidase 4 (DPP-4) inhibitors have been shown to have neuroprotective effects in diabetic patients suffering from stroke, but less research has focused on patients with mild hyperglycemia below the threshold for a diagnosis of diabetes. In this investigation, a hyperglycemic mouse model was generated by intraperitoneal injection of streptozotocin and then subjected to focal cerebral ischemia. We demonstrated that the DPP-4 inhibitor linagliptin significantly decreased the infarct volume, reduced neuronal cell death, decreased inflammation, and improved neurological deficit compared with control mice. Linagliptin up-regulated the expression of p-Akt and p-mTOR and regulated the apoptosis factors Bcl-2, Bax, and caspase 9. Taken together, these results suggest that linagliptin exerts a neuroprotective action likely through activation of the Akt/mTOR pathway along with anti-apoptotic and anti-inflammatory mechanisms. Therefore, linagliptin may be considered as a therapeutic treatment for stroke patients with mild hyperglycemia.
 ...
PMID:DPP-4 Inhibitor Linagliptin is Neuroprotective in Hyperglycemic Mice with Stroke via the AKT/mTOR Pathway and Anti-apoptotic Effects. 3180 42

Stroke is a major cause of mortality and morbidity worldwide. Considerable experimental and clinical evidence suggests that both diabetes mellitus (DM) and post-stroke hyperglycemia are associated with increased mortality rate and worsened clinical conditions in acute ischemic stroke (AIS) patients. Insulin treatment does not seem to provide convincing benefits for these patients, therefore prompting a change of strategy. The selective agonists of Glucagon-Like Peptide-1 Receptors (GLP-1Ras) and the Inhibitors of Dipeptidyl Peptidase-IV (DPP-IVIs, gliptins) are two newer classes of glucose-lowering drugs used for the treatment of DM. This review examines in detail the rationale for their development and the physicochemical, pharmacokinetic and pharmacodynamic properties and clinical activities. Emphasis will be placed on their neuroprotective effects at cellular and molecular levels in experimental models of acute cerebral ischemia. In perspective, an adequate basis does exist for a novel therapeutic approach to hyperglycemia in AIS patients through the additive treatment with GLP-1Ras plus DPP-IVIs.
 ...
PMID:The treament of hyperglycemia in acute ischemic stroke with incretin-based drugs. 3257 26