Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic cerebral infarction is caused primarily by occlusion of a large arterial vessel. Local circulatory disturbances in the center of ischemic tissue and in ischemic penumbra and the degree of sensitivity to ischemia in different brain regions influence subsequent ischemic progression. Postischemic recirculation is impaired by hemodynamic disturbances and formation of microthrombi, hemorrheologic changes and degeneratively altered vessels of microcirculation. Increased postischemic coagulation can be demonstrated in laboratory tests of few minutes extending up to two weeks after the onset of ischemia. Morphological observations on microthrombi after experimental focal ischemia as well as in patients with cerebral infarction show that formation of microthrombi is dependent on the duration of ischemia and the extent of infarcted tissue. Microthrombi are most prevalent in early stages of tissue damage. This suggests that microthrombi have an effect on the progression of ischemic necrosis. On the basis of our results, we can state that 1) microcirculatory disturbances are triggered by focal cerebral ischemia, 2) formation of microthrombi is a contributing factor to the evolution of postischemic microcirculatory disturbances, and 3) microthrombi promote the progression of ischemic necrosis.
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PMID:The role of microthrombi and microcirculatory factors in localization and evolution of focal cerebral ischemia. 203 Aug 32

Background: Ischemic cerebral infarction is a severe clinical condition that can cause serious mortality. Artesunate, an anti-malarial drug that is widely used in cancer treatment, is known to facilitate accelerated cell apoptosis. The aim of this study is to explore the possible neuroprotective effects of artesunate on hypoxic-ischemic cells in rats. Methods: Middle cerebral artery occlusion (MCAO) rats were treated with artesunate in different doses to observe their survival rate. Primary hippocampal neurons were deprived of oxygen-glucose to induce ischemia symptoms. Western blot was performed to determine the protein expressions of p-mTOR, Beclin-1, and Mcl-1. A five-point scale was used to detect neurological deficit. Cell apoptosis was measured using a TUNEL assay. Results: Artesunate supplementation protected MCAO rats from death and ameliorated brain injury among them. Artesunate administration decreased the expression of p-mTOR, increased the expressions of Beclin-1 and Mcl-1, and decreased the activity of caspase-3 in both the rats' ischemia cerebral cortices and their primary ischemia hippocampal neurons when compared with artesunate-absent ischemic brains and cells. The neuroprotective effects of artesunate were abolished by either leucine (LEU) or 3-MA, while the effects of rapamycin were reversed by 3-MA. In vivo experiments verified the protective effects of artesunate on brain-infarct rats. Conclusion: The results indicate the protectiveness of artesunate against ischemic cerebral infarction, whereas the protectiveness might increase autophagy through regulating the activity of mTOR.
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PMID:Protectiveness of Artesunate Given Prior Ischemic Cerebral Infarction Is Mediated by Increased Autophagy. 3017 40