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)

Intracerebral injection of the vasoconstrictor peptide, endothelin-1 (ET-1), has been used as a method to induce focal ischemia in rats. The relative technical simplicity of this model makes it attractive for use in mice. However, the effect of ET-1 on mouse brains has not been firmly established. In this study, we determined the ability of ET-1 to induce focal cerebral ischemia in four different mouse strains (CD1, C57/BL6, NOD/SCID, and FVB). In contrast to rats, intracerebral injection of ET-1 did not produce a lesion in any mouse strain tested. A combination of ET-1 injection with either CCA occlusion or N(G)-nitro-l-arginine methyl ester (l-NAME) injection produced only a small infarct and its size was strain-dependent. A triple combination of CCA occlusion with co-injection of ET-1 and l-NAME produced a lesion in all mouse strains tested, and this resulted in a significant motor deficit. However, lesion size was still relatively small and strain-dependent. This study shows that ET-1 has a much less potent effect for producing an infarct in mice than rats.
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PMID:Mouse model of focal cerebral ischemia using endothelin-1. 1862 Oct 79

In order to evaluate novel stroke therapies, it is essential to utilize a highly reproducible model of focal cerebral ischemia. Though a range of rodent stroke models has been employed in the literature, there are persistent issues regarding reproducibility of the ischemic zone, as there is considerable inter-animal and inter-laboratory variation. We have developed a highly reproducible model of stroke that involves direct electrocoagulation of the MCA in SCID (CB-17/lcr-scid/scidJcl) and CB-17 (CB-17/lcr-+/+Jcl) mice. Using a modification of the Tamura method, our results demonstrate reproducible cortical infarction with high survival in the chronic period (up to 180 days) in SCID and CB-17, but not in C57BL/6, mice. We believe that our preclinical model represents a step forward for testing future therapeutic methods potentially applicable to patients with stroke.
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PMID:A Reproducible and Simple Model of Permanent Cerebral Ischemia in CB-17 and SCID Mice. 2086 60

Previous studies have shown that Bererine (Ber) has significant neuroprotective effects and the present article aimed to investigate its mechanism from the aspect of peripheral immune system. We evaluated the effects of Ber 24 h after cerebral ischemia/reperfusion (I/R) on histologic injury in BALB/C mice and NOD-SCID (severe combined immunodeficient) mice lacking T and B cells. Infarct volume, neurological scores and brain water content were strikingly reduced by Ber in BALB/C mice versus NOD-SCID mice. Which suggested that Ber induces peripheral immune regulations to realize its neuroprotective effects in the cerebral I/R mice. Then we tested the lymphocytes from BALB/C lymph nodes (LNs) with their survival, activation, proliferation, cell cycle, apoptosis and differentiation induced by cytokine secretion to provide direct evidences that Ber realized its neuroprotective effects by regulating I/R-induced peripheral lymphocytes early immunoactivation and following immunotolerance and to better understand the importance of peripheral immune system following I/R insults.
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PMID:Bererine induces peripheral lymphocytes immune regulations to realize its neuroprotective effects in the cerebral ischemia/reperfusion mice. 2257 86