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Biosci Biotechnol Biochem ; 84(12): 2476-2483, 2020 Dec.
Artículo en Inglés | MEDLINE | ID: mdl-32815784

RESUMEN

This work aimed to assess the role of TLR8 in cerebral I/R injury and its in-depth pathogenesis. Bioinformatics analysis indicated that TLR8 was up-regulated in patients with ischemic stroke than that in healthy control, and miR-18a-5p was the upstream regulatory of TLR8. Then, the rat pheochromocytoma PC12 cells were exposed in oxygen-glucose-deprivation/reoxygenation (OGD/R) conditions to construct a model in vitro. The functional experiments indicated that OGD/R can decline the viability and elevate the apoptosis of PC12 cells, while up-regulation of miR-18a-5p can alleviate OGD/R-induced cell injury. Notably, overexpression of TLR8 reverses the miR-18a-5p-mediated protection on OGD/R-induced cells injury. Finally, we found that up-regulation of miR-18a-5p obviously declined the protein levels of TLR4 and TLR7 as well as the phosphorylation of NF-κB, while overexpression of TLR8 canceled the decrease caused by miR-18a-5p up-regulation. In summing, our results illustrated that miR-18a-5p/TLR8 axis can mitigate OGD/R-induced cells injury through TLRs and NF-κB pathway.


Asunto(s)
Glucosa/metabolismo , MicroARNs/genética , FN-kappa B/metabolismo , Oxígeno/metabolismo , Transducción de Señal/genética , Receptor Toll-Like 8/metabolismo , Animales , Supervivencia Celular/genética , Técnicas de Silenciamiento del Gen , Humanos , Accidente Cerebrovascular Isquémico/genética , Accidente Cerebrovascular Isquémico/metabolismo , Accidente Cerebrovascular Isquémico/patología , Células PC12 , Ratas , Transducción de Señal/efectos de los fármacos , Receptor Toll-Like 8/deficiencia , Receptor Toll-Like 8/genética
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