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)

Omega-3 polyunsaturated fatty acids (PUFA n3) provide neuroprotection due to their anti-inflammatory and anti-apoptotic properties as well as their regulatory function on growth factors and neuronal plasticity. These qualities enable PUFA n3 to ameliorate stroke outcome and limit neuronal damage. Young adult male rats received transient middle cerebral artery occlusion (tMCAO). PUFA n3 were intravenously administered into the jugular vein immediately after stroke and 12h later. We analyzed stroke volume and behavioral performance as well as the regulation of functionally-relevant genes in the penumbra. The extent of ischemic damage was reduced and behavioral performance improved subject to applied PUFA n3. Expression of Tau and growth-associated protein-43 genes were likewise restored. Ischemia-induced increase of cytokine mRNA levels was abated by PUFA n3. Using an in vitro approach, we demonstrate that cultured astroglial and microglia directly respond to PUFA n3 administration by preventing ischemia-induced increase of cyclooxygenase 2, hypoxia-inducible factor 1alpha, inducible nitric oxide synthase, and interleukin 1beta. Cultured cortical neurons also appeared as direct targets, since PUFA n3 shifted the Bcl-2-like protein 4 (Bax)/B-cell lymphoma 2 (Bcl 2) ratio towards an anti-apoptotic constellation. Thus, PUFA n3 reveal a high neuroprotective and anti-inflammatory potential in an acute ischemic stroke model by targeting astroglial and microglial function as well as improving neuronal survival strategies. Our findings signify the potential clinical feasibility of PUFA n3 therapeutic treatment in stroke and other acute neurological diseases.
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PMID:Omega-3 polyunsaturated fatty acids ameliorate neuroinflammation and mitigate ischemic stroke damage through interactions with astrocytes and microglia. 2546 70

Neurological functions were seriously impaired by cerebral ischemia-reperfusion (I/R) injury following ischemic stroke and its molecular mechanism is still not fully understood. MicroRNA-496 (miR-496) has been reported to be deregulated in several diseases but it still remains unknown about the function of miR-496 in cerebral I/R injury. Here, Middle cerebral artery occlusion/reperfusion (MCAO/R) was performed to induce cerebral I/R injury in rats. Then, neurological deficits were assessed by Bederson and Longa score system. The 2,3,5-triphenyltetrazolium chloride (TTC) and terminal deoxynucleotidyltransferase UTP nick end labeling (TUNEL) staining were used to evaluate the rat brain pathology. The oxygen-glucose deprivation and reperfusion (OGD/R) induced in vitro I/R injury was constructed in SH-SY5Y cells. The expression of miR-496 was determined using Real-time PCR. Bioinformatics analysis and dual luciferase reporter assay were utilized to confirm the target gene of miR-496. CCK-8, EdU staining, flow cytometry and Hoechst 33258 staining were respectively utilized to measure cell viability, proliferation and apoptosis. The results showed the expression of miR-496 was found to be down-regulated by cerebral I/R in rats and OGD/R-inducedSH-SY5Y cell model. MiR-496 overexpression alleviated the OGD/R-induced injury in SH-SY5Y cells. In addition, pro-apoptosis factor Bcl-2-like protein 14 (BCL2L14) was predicted and verified as the direct target of miR-496 and suppressed by miR-496. Furthermore, BCL2L14 knockdown exhibited similar effects similar to those of miR-496 overexpression, and the restored BCL2L14expression reversed the protective effects of miR-496 on SH-SY5Y cells. In conclusions, our results suggest that miR-496 alleviates cerebral I/R injury possibly via inhibiting BCL2L14 expression.
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PMID:Upregulation of miR-496 decreases cerebral ischemia/reperfusion injury by negatively regulating BCL2L14. 3059 31