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

This study examined the neuroprotective effects and possible hepatotoxicity of (-)-epigallocatechin gallate (EGCG) in a rat model of transient focal cerebral ischemia. Male Sprague-Dawley rats (265-295 g) were treated with either 50 mg kg(-1) of EGCG or saline, i.p., immediately post-ischemia and every day thereafter, in a middle cerebral artery occlusion model of stroke. Sacrifice occurred 72 h post-ischemia and 2,3,5-triphenyltetrazolium chloride staining was used to quantify neuronal infarction. Hepatotoxicity was determined by taking blood samples for plasma alanine aminotransferase (ALT) activity. Spleen, kidney, liver and testes wet weights were also recorded. Total infarct volume was significantly (P<0.05) reduced in the EGCG-treated group as compared to controls. Analysis of the mean infarct area showed a significant (P<0.05) decrease in slices 6 and 7 in the EGCG-treated group. No significant differences were found in organ weights or ALT levels between treatment groups. Our findings, in part, validate and extend previous observations illustrating that 50 mg kg(-1), i.p. EGCG is non-toxic and neuroprotective. However, we also found that EGCG treatment appreciably increased (>50%) the number of animals that developed an intracerebral hemorrhage. We therefore conclude that 50 mg kg(-1) EGCG is not a viable intervention for the acute treatment of cerebral ischemia, as it is likely to increase the risk of intracerebral hemorrhaging.
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PMID:(-)-Epigallocatechin gallate as an intervention for the acute treatment of cerebral ischemia. 1592 95

Cerebral ischemia, a phenomenon of reduction in cerebral blood flow, accounts for approximately 80% of all strokes, the third leading cause of death and the leading cause of adult disability. Cerebral ischemia causes heterogeneous changes in tissue oxygenation and cellular metabolism. Focal brain ischemia induces a profound and long-lasting inflammatory reaction which is dominated by macrophages derived from both resident microglia and circulating monocytic precursors. Bone marrow and spleen serve as a reservoir for hematopoietic progenitor cells, especially in rodents. Spleen-derived mononuclear cells home to the site of vascular injury and reduced neointima formation. The migration and engraftment of systematically administered spleen-derived mononuclear cells can be visualized in the post-ischemic brain. Therefore, we hypothesise that removal of the spleen may possibly decrease the production of mononuclear cells, and thus hinder or relieve the inflammatory reaction occured after cerebral ischemia/reperfusion injury. So, the splenectomy may be a prophylactic treatment method for cerebral ischemia.
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PMID:Splenectomy may be a prophylactic treatment for cerebral ischemia? 2038 Dec 61

NDRG4 is a member of the NDRG family (N-myc downstream-regulated gene), which is highly expressed in brain and heart. Previous studies showed that Ndrg1-deficient mice exhibited a progressive demyelinating disorder of peripheral nerves and Ndrg4-deficient mice had spatial learning deficits and vulnerabilities to cerebral ischemia. Here, we report generation of Ndrg4 mutant alleles that exhibit several development defects different from those previously reported. Our homozygous mice showed growth retardation and postnatal lethality. Spleen and thymuses of Ndrg4(-/-) mice are considerably reduced in size from 3 weeks of age. Histological analysis revealed abnormal hyperkeratosis in the squamous foregut and abnormal loss of erythrocytes in the spleen of Ndrg4(-/-) mice. In addition, we observed an abnormal hind limb clasping phenotype upon tail suspension suggesting neurological abnormalities. Consistent to these abnormalities, Ndrg4 is expressed in smooth muscle cells of the stomach, macrophages of the spleen and neurons. Availability of the conditional allele for Ndrg4 should facilitate further detailed analyses of the potential roles of Ndrg4 in gut development, nervous system and immune system.
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PMID:Postnatal lethality and abnormal development of foregut and spleen in Ndrg4 mutant mice. 2680 54