The expression and functions of microRNA (miR)-411 have been investigated in several types of cancer. However, until now, miR-411 in human breast cancer has not been examined. The present study investigated the expression, biological functions and molecular mechanisms of miR-411 in human breast cancer, discussing whether it offers potential as a therapeutic biomarker for breast cancer in the future. The expression levels of miR-411 in human breast cancer tissues and cells were measured using reverse transcription-quantitative polymerase chain reaction analysis. Following transfection with miR-411 mimics, an MTT assay, cell migration and invasion assay, western blot analysis and luciferase assay were performed in human breast cancer cell lines. According to the results, it was found that miR-411 was significantly downregulated in breast cancer, and associated with lymph node metastasis and histological grade. Additionally, it was observed that miR-411 suppressed cell growth, migration and invasion in the breast cancer cells. The present study also provided the first evidence, to the best of our knowledge, that miR-411 was likely to directly target specificity protein 1 in breast cancer. These findings indicated that miR-411 may be used a therapeutic biomarker for the treatment of breast cancer in the future.
Objective
To investigate whether irisin could protect against blood–brain barrier (BBB) dysfunction following focal cerebral ischemia/reperfusion in rats.
Methods and Materials
Seventy‐two adult male Sprague Dawley rats weighing 280–320 g were randomly divided into three groups: sham operation group (S), focal cerebral ischemia/reperfusion group (FC), and irisin group (IR). Focal cerebral ischemia was induced by improved thread occlusion of right middle cerebral artery (MCAO) for 2 hr followed by reperfusion for 24 hr in rats. After 24 hr of reperfusion, the neurological evaluation was performed by the method of Longa's score. The histopathological changes were observed by HE staining. The brain water content was determined by detecting the wet weight and dry weight. The BBB permeability was assessed by fluorescence spectrophotometer and fluorescence microscopy for Evans blue (EB) extravasation. The activity and expression of matrix metalloproteinase‐9 (MMP‐9) in different groups were detected by immunohistochemical staining, Western blot, and gel gelatin zymography.
Results
After MCAO, the neurological deficit scores, the infarct volume, the brain water content, and the EB content were higher in the FC group than those in the S group (p < .05). While after irisin treatment, these indicators mentioned above were lower than those in the IR group (p < .05). Moreover, the protein expression of MMP‐9 in the cortex increased significantly after MCAO, while irisin treatment could decrease the protein expression of MMP‐9 in the cortex (p < .05).
Conclusion
Our data suggest that irisin can attenuate brain damage both morphologically and functionally and protect BBB from disruption after focal cerebral ischemia/reperfusion, which is highly associated with the inhibition of the expression and activity of MMP‐9 in the brain tissue.
Methylene blue (MB) is a long-term inhibitor of peripheral nerve axons, thereby alleviating or permanently eliminating pain. However, it remains unknown whether MB is safe and effective method of treating osteoarthritis (OA). MB was injected into the knee joints of rabbits and they were monitored for any histological structural changes. The results revealed no evident changes in the histological structure of the normal knee joint following injection of 1 mg/kg MB at 1, 4, 8 and 24 weeks post-injection. Compared with the vehicle control, MB treatment significantly enhanced the weight distribution and significantly decreased the swelling ratio of the rabbits. Additionally, levels of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) mRNA were significantly increased following treatment with MB, but the protein expression of P2X purinoceptor 3 (P2X3) was significantly suppressed compared with the vehicle control. The levels of interleukin (IL) 6, tumor necrosis factor (TNF)α, IL-1β and IL-8 were significantly suppressed following MB treatment, indicating that MB protects against OA progression. It was also revealed that MEG3 overexpression significantly suppresses levels of P2X3 protein. ELISA indicated that the MEG3-induced reduction of IL-6, TNFα, IL-1β and IL-8 expression was significantly reversed following P2X3 overexpression. Therefore, the results of the present study demonstrated that MB is an effective method of treating OA-associated pain by upregulating lncRNA MEG3 levels. Additionally, lncRNA MEG3 relieves the OA-associated pain and inflammation in a rabbit model of OA by inhibiting P2X3 expression.
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