A meta-analysis of comparisons of various surgical treatments for moyamoya diseases.

PURPOSE: Ischemia is one of the most familiar complications in the different procedures for moyamoya disease (MMD), but the optimal surgical approaches for MMD remain unknown. We aimed to evaluate the efficiency of various surgical treatments. METHODS: A literature search word was performed through four databases such as Cochrane Library, Web of Science, PubMed, and EMBASE for the literature published until May 2021. The I2 statistic was used to assess heterogeneity. A random/fixed-effects model was used to pool. RESULTS: There are a total of 18 studies including three surgical treatments such as including indirect, direct, and combined bypass in this study. The result revealed that indirect bypass was related to a higher incidence of recurrence stroke compared to the direct and combined bypass treatment (p = .001). Furthermore, the cases undergoing direct bypass were associated with a better angiographic change than the indirect bypass (OR = 3.254, p = .013). CONCLUSION: This meta-analysis demonstrated a positive effect of using the direct and combined bypass to treat MMD compared to indirect bypass due to their lower rates of recurrence stroke.

Osthole suppresses the proliferation and accelerates the apoptosis of human glioma cells via the upregulation of microRNA-16 and downregulation of MMP-9.

Osthole (7-methoxy-8-isoamyl alkenyl coumarin) has been reported to exhibit marked anticancer effects on several types of cancer. The expression levels of matrix metalloproteinase-9 (MMP-9) are closely associated with the pathogenesis of glioma. Furthermore, it is reported that the upregulation of microRNA­16 (miR­16) by the MMP­9 signaling pathway can restrain the proliferation of cancer cells. To examine whether osthole increases the anticancer effect on human glioma cells in the present study, the common glioma cell line, U87, was treated with osthole at concentrations of 0, 50, 100 and 200 µΜ. The effects of osthole on cell viability were determined using a 3­(4,5­dimethylthiazol­2­thiazolyl)­2,5­diphenyl­tetrazolium bromide assay. The rate of cellular apoptosis was analyzed by measuring the activity of caspase­3 and using flow cytometry. The expression of MMP­9 was determined using gelatin zymography assays and the expression of miR­16 was determined using reverse transcription­quantitative polymerase chain reaction. The results demonstrated that osthole significantly suppressed the proliferation and accelerated the apoptosis of the U87 cells. Furthermore, increased expression levels of miR­16 and reduced protein expression levels of MMP­9 were found in the U87 cells. In addition, miR­16 was found to regulate the expression of MMP­9 in the U87 cells through transfection of miR­16 precursor and anti­miR­16 into the U87 cells. In conclusion, these observations indicated that osthole suppressed the proliferation and accelerated the apoptosis of human glioma cells through upregulation of the expression of miR­16 and downregulation of the expression of MMP-9.

In vitro studies of phenethyl isothiocyanate against the growth of LN229 human glioma cells.

Phenethyl isothiocyanate (PEITC) is one of the best studied members of isothiocyanates (ITC), a variety of edible cruciferous vegetables including broccoli, watercress, and cabbage, and have generated particular interest because of its remarkable chemopreventive activity. Many literature reports proved that phenethyl isothiocyanate exhibited significant anti-cancer chemopreventive effects including lung, glioma and leukemia cancer. In this study, we explored the inhibitory effects as well as mechanisms of PEITC on human glioma LN229 cells. Results demonstrated that PEITC possesses the potential ability to inhibit proliferation, induce apoptosis and arrest cell cycling against LN229 human glioma cells. Moreover, investigated results showed that PEITC inhibited the expression of superoxide dismutase (SOD) and glutathione (GSH), and caused oxidative stress to tumor cells. Collective results suggested us to believe that PEITC can inhibit the growth of LN229 cells and its mechanism can be related to the fact that PEITC can cause oxidative stress to tumor cells.

Cilostazol induces mitochondrial fatty acid ß-oxidation in C2C12 myotubes.

Cilostazol is a drug licensed for the treatment of intermittent claudication. Its main action is to elevate intracellular levels of cyclic monophosphate (cAMP) by inhibiting the activity of type III phosphodiesterase, a cAMP-degrading enzyme. The effects of cilostazol on fatty acid oxidation (FAO) are as yet unknown. In this study, we report that cilostazol can elevate complete FAO and decrease both triacylglycerol (TAG) accumulation and TAG secretion. This use of cilostazol treatment increases expression of PGC-1α and, subsequently, its target genes, such as ERRα, NOR1, CD36, CPT1, MCAD, and ACO. Expression of these factors is linked to fatty acid ß-oxidation but this effect is inhibited by H-89, a specific inhibitor of the PKA/CREB pathway. Importantly, knockdown of PGC-1α using siRNA abolished the effects of cilostazol in fatty acid oxidation (FAO) and TAG metabolism. These findings suggested that the PKA/CREB/PGC-1α pathway plays a critical role in cilostazol-induced fatty acid oxidation and TAG metabolism.