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)

Cerebral ischemia induces many degenerative cellular reactions, including the release of excitatory amino acids, the formation of oxygen free radicals, Ca2+ overload, the activation of several cellular enzyme systems such as Ca2+ dependent proteases, and the initiation or genomic responses that can affect the tissue outside the area of reduced blood flow. Furthermore, increasing evidence indicates that apoptosis contributes to the death of brain cells following cerebral ischemia. Several studies have shown that cerebral ischemia alters the expression of genes, some of which may play protective or harmful roles. Although many genes have the potential to treat cerebral ischemia, target genes or their translated products are often difficult to express, if at all, in brain cells. However, adenovirus-mediated gene transfer can overcome this disadvantage. To date, many treatment strategies have been developed for cerebral ischemia using target genes such as neuronal apoptosis inhibitory protein (NAIP), glial cell line-derived neurotrophic factor (GDNF), sensitive to apoptosis gene (SAG), 150-kDa oxygen-regulated protein (ORP150), etc. Moreover, new vectors and gene delivery systems are constantly being invented although there is no perfect vector to date. Gene therapy could constitute a powerful strategy to treat cerebral ischemia in the near future.
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PMID:Recent advances in adenovirus-mediated gene therapy for cerebral ischemia. 1255 34

Previous experiments showed that ginsenoside Rb1 (GRb1) reduced infarct and neuronal deficit in rats followed by transient cerebral ischemia. The mechanism of this neuroprotective function is unclear. Here, we tested whether the effect of GRb1 can be achieved through preventing ischemic neuronal death, modulating apoptotic-related genes and affecting glial-derived neurotrophic factor (GDNF) expression in rats subjected to occlusion of the middle cerebral artery. When GRb1(40 mg/kg, i.p.) was administered immediately after reperfusion, the apoptotic cells in the GRb1 group were decreased significantly from 12 to 72 h of reperfusion compared to the ischemia group by TdT-mediated dUTP-biotin nick-end labeling. Immunostaining and Western blotting analysis showed that the expression of GDNF from 3 to 120 h of the GRb1 group was significantly increased compared to the ischemia group, and GDNF expression peaked at 48 h after reperfusion. The enhanced GDNF mRNA in the GRb1 group was not detected by RT-PCR and in situ hybridization compared to the ischemia group, but GDNF mRNA at 48 h after reperfusion was strongly increased in both the ischemia and GRb1 group when compared to other time points. The number of bcl-2-positive cells was significantly increased from 12 to 120 h of reperfusion compared to the ischemia group. However, the number of bax-positive cells in the GRb1 group was significantly declined compared to the ischemia group. In the GRb1 group, the number of neuronal apoptosis inhibitory protein-positive cells from 12 to 120 h after reperfusion was evidently higher than that in the ischemia group. Therefore, ginsenoside Rb1 prevents ischemic neuronal death induced by transient cerebral ischemia, and this mechanism of which is related to increase the expression of the antiapoptotic genes and modulate the expression of GDNF.
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PMID:Neuroprotective effects of ginsenoside Rb1 on transient cerebral ischemia in rats. 1766 84