AIM: To study miR-24 effects on cerebral infarction in rats. MATERIAL and METHODS: A rat middle cerebral artery occlusion model (MCAO) was constructed. Intracerebroventricular stereotactic injection of miR-24 agomir/antagomir was performed in the rat MCAO model. According to different experiences, rats were divided into normal, sham, MCAO, miR-24 agomir and miR-24 antagomir groups. Serum TCH, HDL and TG levels were detected. RESULTS: Comparingthe normal and sham groups, we observed decreased relative miR-24 expression (P< 0.05) and increased cerebral infarction area percentage, apoptotic cells and relative caspase-3 protein expression (P< 0.05) in theMCAO, miR-24 agomirand miR-24 antagomir groups. TC, TG and HDL-C levels of the MCAO and miR-24 antagomir groups were higher than those of normal and sham groups (P< 0.05).Compared with the MCAO group, increased relative miR-24 expression (P< 0.05) and decreased TC, TG and HDL-C levels,cerebral infarction area percentage, number of apoptotic cells and caspase-3 expression (P< 0.05) were found in themiR-24 agomir group, contrasting with theobservations from the miR-24 antagomir group. CONCLUSION: miR-24 reduced serum TCH, HDL and TG levels and inhibited brain tissue cell apoptosis in rats with cerebral infarction.

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MiRNAs are emerging as important epigenetic modulators of multiple target genes, leading to abnormal cellular signaling involving cellular proliferation in cancers. Aberrant miRNA expression has been observed in human glioblastoma (GBM). The present study was to evaluate the expression and molecular mechanisms of COX-2 and miR-26b in human GBM tissues and GBM cell lines T98G, U87 and U251. In the present study, we found that expression of miR-26b was markedly downregulated in GBM cell lines and human GBM tissues, compared to matched non-tumor associated tissues. Furthermore, miR-26b expression was inversely proportional to that of COX-2 mRNA and protein. Ectopic expression of miR-26b dramatically reduced the proliferation, colony formation, and proliferation/apoptosis-related proteins in GBM cells. Flow cytometry analysis showed that ectopic expression of miR-26b significantly decreased the percentage of S phase cells and increased the percentage of G1/G0 phase cells. Finally, luciferase reporter assay revealed that miR-26b inhibited the expression of COX-2 by binding to the 3'-UTR of COX-2 in GBM cells. Taken together, our results suggest that miR-26b plays an important role to inhibit the proliferation and invasion of GBM cells, and presents a novel mechanism for direct miR-26bmediated suppression of COX-2 in GBM. Thus, miR-26b/COX-2 may have an important role in treatment of GBM patients.