RESUMO
To investigate the expression of miR-203 by sevoflurane treatment and its effect on neuroinflammation induced by cerebral ischemia-reperfusion. Rats were randomly divided into sham operation group (C), cerebral ischemia-reperfusion group (I/R), and sevoflurane treatment group (S). The neurological function score was evaluated. The area of cerebral infarction was evaluated by TTC staining. The expression of inflammatory factor in brain tissue was detected by ELISA. The apoptosis of neurons was detected by TUNEL. A miR-203 agonist and inhibitor treated the cerebral ischemia-reperfusion model. The luciferase assay verified whether miR-203 targeted MyD88. To further verify the relationship between miR-203 and MyD88, the I/R group was treated with MyD88 activator and inhibitor, and the mRNA expressions of miR-203 and MyD88 in brain tissue were detected by RT-PCR. Western blot was used to detect the expression of MyD88 protein in brain tissue, and the above experiment was repeated. Compared with the I/R group, miR-203 mRNA was significantly increased in brain tissue and the neurological function score, the area of cerebral infarction, the expression of inflammatory factor, and MyD88 mRNA were decreased in the S group (P < 0.05). After treatment of miR-203 agonist and inhibitor in the I/R group, overexpression of miR-203 could alleviate cerebral ischemia-reperfusion injury, and miR-203 inhibitor could aggravate cerebral ischemia-reperfusion injury. The miR-203 agonist could enhance the action of sevoflurane, and the miR-203 inhibitor could reverse the action of sevoflurane. miR-203 agonist treatment could inhibit the expression of MyD88 gene and protein and reduce the neuroinflammation induced by cerebral ischemia-reperfusion. The treatment of sevoflurane upregulated miR-203 expression, which targeted MyD88 and attenuate neuroinflammation induced by cerebral ischemia-reperfusion.
