Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, we investigated the effects of electroacupuncture (EA) on ischemia-induced neurogenesis in the striatum of adult rat brains with a 30-minute middle cerebral artery occlusion. Injection of bromodeoxyuridine (BrdU, 30 mg/kg, i.p., cell proliferation marker) and 1,1'-dioctadecyl-6,6'-di(4-sulfophenyl)-3,3',3',3' -tetramethylindocarbo-cyanine (DiI, 1 microg/ microl, i.c.v, lipophilic neuronal tracer) combined with multiple fluorescence immunostaining were used to determine whether the proliferated cells were newly generated neurons and where they originated from in the brain. We demonstrated that EA treatment (60 Hz 1 s and 2 Hz 3 s alternately at an intensity of 10 mA for 20 min on "Fengfu", GV.16 and "Jinsuo", GV.8) enhanced stroke-induced striatal neurogenesis in rat brains as follows: 1) EA increased the number of BrdU+ cells, indicating that it activates cell proliferation; 2) EA increased BrdU+/CRMP-4(+) (collapsing response mediated protein-4, immature neuron marker) and BrdU+/MAP-2(+) (microtubule-associated protein 2, mature neuron marker) cells, suggesting that it facilitates neurogenesis and maturation of newly generated neurons; 3) EA expanded the distribution of DiI-stained cells in the striatum. Moreover, most BrdU+/CRMP-4(+) or BrdU+/MAP-2(+) cells in the striatum were observed DiI+ staining. Thus, the results suggest that striatal newborn neurons mainly migrate from the cells lining ventricle. Therefore, we conclude that EA can improve neuronal regeneration, newborn neuron migration and their maturation in the striatum of adult rat brains after stroke.
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PMID:Electroacupuncture enhances striatal neurogenesis in adult rat brains after a transient cerebral middle artery occlusion. 1661 87

To elucidate whether vascular endothelial growth factor (VEGF) improves stroke-induced striatal neurogenesis, we intraventricularly injected human VEGF(165)-expressive plasmid (phVEGF) mixed with liposome into adult rats after a transient middle cerebral artery occlusion (MCAO). The results showed that EGFP, a reporter protein, positive cells appeared at 2 hr, further enhanced at 4 hr, reached the maximum at 3 days and still remained at 14 days after a single injection. Treatment with phVEGF increased angiogenesis, as indicated by double staining of vWF, a marker of endothelial cells, and 5'-bromodeoxyuridine (BrdU), a marker of cell proliferation. The phVEGF treatment dose-dependently reduced infarct volume of brain at 2 weeks after MCAO. The neuroprotection by VEGF could be obtained when the plasmid was injected within 2 hr after stroke. Moreover, VEGF overexpression significantly increased cell proliferation in the ipsilateral SVZ and the numbers of BrdU(+)-CRMP-4(+) and BrdU(+)-Tuj1(+), two markers of immature newborn neurons, and BrdU(+)-MAP-2(+), a marker of mature newborn neurons, cells in the ipsilateral striatum to MCAO. Present results show that VEGF plasmid treatment after stroke can significantly reduce infarct volume and enhance striatal neurogenesis in adult rat brain. This suggests that VEGF overexpression acquires significant functions of neuronal protection and repair in the injured brain, which provides a possibility to develop a novel therapeutic strategy for the patients with stroke.
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PMID:VEGF overexpression enhances striatal neurogenesis in brain of adult rat after a transient middle cerebral artery occlusion. 1706 Dec 57

In this research, we investigated striatal neurogenesis in 3-, 6-, 12-, and 18-month-old rats after cerebral ischemic injury. All rats were subjected to a 20-min middle cerebral artery occlusion (MCAO), given 5'-bromodeoxyuridine (BrdU, 30 mg/kg, i.p.) once daily during days 4-7 and sacrificed 2 weeks after MCAO. Neurogenesis was assessed with double immunohistochemical/immunofluorescence labeling of BrdU and doublecortin (DCX), microtubule-associated protein 2 (MAP-2), or 67-kDa glutamic acid decarboxylase (GAD(67)). In 6-, 12-, and 18-month-old rats, the numbers of nestin(+), BrdU(+)-DCX(+) (a marker of newborn neuronal progenitors/immature neuron), BrdU(+)-MAP-2(+) (a marker of newborn mature neuron), and BrdU(+)-GAD(67)(+) (a marker of newborn GABAergic neuron) cells decreased dramatically in the ipsilateral striatum to MCAO compared with that in 3-month-old rats. The results indicated that stroke-induced striatal neurogenesis still existed in aging rats. However, the capacity of neurogenesis in older rats was considerably lower than that in young adults. Meanwhile, the apoptosis of neural precursors and immature neurons, indicated by double labeling of active caspase-3 and nestin/DCX/Tuj-1(beta-tubulin III)/CRMP-4 (collapsin response-mediated protein-4), increased noticeably in the ipsilateral striatum of older rats. Taken together, the results suggested that aging-related attenuation of ischemia-induced striatal neurogenesis might be related to decrease of neural precursors and increase of apoptosis of newborn neurons.
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PMID:Age-related decrease of striatal neurogenesis is associated with apoptosis of neural precursors and newborn neurons in rat brain after ischemia. 1766