Propofol exerts neuroprotective functions by down-regulating microRNA-19a in glutamic acid-induced PC12 cells.

BACKGROUND: Propofol, a kind of intravenous sedative drug, is certified that exerts anti-inflammation and antitumor functions. However, the influence of propofol in cerebral injury and the corresponding mechanism remains unexplained, that our article focuses on. METHODS: PC12 cells were treated with propofol and exposed in glutamic acid (Glu) solutions. Cell viability, apoptotic potential, apoptosis-related and autophagy-linked proteins were tested via CCK-8, flow cytometry, and western blot assays. Reverse transcription-quantitative real-time PCR was utilized to test miR-19a expression in Glu-stimulated cells. Next, miR-19a mimic transfection was used to assess the effects of miR-19a on cell apoptosis and autophagy in Glu or propofol treated cells. Finally, western blot was performed to test AMPK and mTOR pathways. RESULTS: Glu exposure promoted cell apoptosis and autophagy of PC12 cells, while propofol attenuated cell apoptosis and autophagy triggered by Glu. Additionally, propofol decreased the miR-19a expression in Glu-stimulated PC12 cells. Meanwhile, over-expression of miR-19a reversed the effects of propofol on Glu-induced cell apoptosis and autophagy. Moreover, propofol potentiated AMPK and mTOR pathways in Glu-stimulated PC12 cells via impeding miR-19a expression. CONCLUSIONS: These finding revealed that propofol relieved Glu-triggered apoptosis and autophagy of PC12, and activated AMPK and mTOR pathways by suppressing miR-19a expression.

Evaluation of local anesthetic effects of Lidocaine-Ibuprofen ionic liquid stabilized silver nanoparticles in Male Swiss mice.

A simple approach for the synthesis of Lidocaine-Ibuprofen ionic liquid stabilized silver nanoparticles (IL-AgNPs) was reported in this work. The shape, size and surface morphology of the Lidocaine-Ibuprofen ionic liquid stabilized AgNPs were characterized by using spectroscopic and microscopic techniques such as Ultraviolet-visible spectroscopy (UV-Visible), X-ray diffraction (XRD) analysis, Selected area electron diffraction (SAED), Transmission electron microscopy (TEM). TEM analysis showed the formation of 20-30nm size of IL-AgNPs with very clear lattice fringes. SAED pattern confirmed the highly crystalline nature of fabricated IL stabilized AgNPs. EDS results confirmed the formation of nanosilver. The fabricated IL-AgNPs were studied for their local anesthetic effect in rats. The results of local anesthetic effect showed that the time for onset of action by IL-AgNPs is 10min, which is significantly higher than that for EMLA. Further, tactile test results confirmed the stronger and faster local anesthetic effect of IL-AgNPs when compared to that of EMLA.

MicroRNA-193b inhibits the proliferation, migration and invasion of gastric cancer cells via targeting cyclin D1.

MicroRNAs have been involved in RNA silencing and post-transcriptional regulation of gene expression and also play important roles in tumorigenesis and tumor progression. MiR-193b was previously reported to act as tumor suppressor in diverse cancers. However, little is known about the expression, function and mechanism of miR-193b in gastric cancer (GC). In this study, we investigated the expression of miR-193b in 50 GC cases and found that miR-193b was significantly reduced in GC tissues compared with the adjacent normal gastric tissues. Moreover, lower-level of miR-193b was also associated with a more aggressive GC phenotype. We further demonstrated that miR-193b can inhibit the proliferation, migration and invasion of HGC-27 and MGC-803 GC cells. Further mechanism study indicated that CCND1 was a direct target of miR-193b in GC. Overexpression of miR-193b inhibited the expression of CCND1, and knock-down of CCND1 inhibited the proliferation of GC cells, suggesting that miR-193b exerted its anti-tumorigenic role in GC cells through targeting CCND1 gene.