Crocin regulates the proliferation and migration of neural stem cells after cerebral ischemia by activating the Notch1 pathway.

INTRODUCTION: To investigate the effects of crocin on proliferation and migration of endogenous neural stem cells and the Notch1 signalling pathway in rats after cerebral ischemia reperfusion. MATERIAL AND METHODS: SD rats were randomly divided into the sham operation group, model group and administration group (crocin). Middle cerebral artery occlusion (MCAO/R) was used to establish the focal cerebral ischemia reperfusion model in rat. After surgical treatment, the treatment group was treated with crocin. Quantitative polymerase chain reaction (qPCR) was used to detect the changes in the expression of Notch1, Bax and bcl-2 proteins in rat endogenous neural stem cells after cerebral ischemia reperfusion. ELISA was used to detect changes in inflammatory factors. Neural stem cells were cultured in vitro, which were divided into: the normal control group, the hypoglycaemic deprivation/reoxygenation group, hypoglycaemic deprivation/reoxygenation group with a low concentration of crocin, and hypoglycaemic deprivation/reoxygenation group with a high concentration of crocin. The cell proliferation assay detects cell activity. The cell migration assay tests the cell migration ability. And flow cytometry was used to determine cell apoptosis. RESULTS: Compared with the sham group, the Notch1 signalling pathway was activated in the model group. The expression of Notch1 in the crocin group was increased compared to the model group. Crocin can inhibit the release of inflammatory factors. The results of our experiments showed that crocin could induce the proliferation and migration of neural stem cells and inhibit the apoptosis of neural stem cells in the hypoglycaemic/reoxygenation model group. CONCLUSIONS: Crocin sufficiently promotes the proliferation and migration of neural stem cells and inhibits the apoptosis of these cells in rats after ischemia-reperfusion by manipulating the Notch signalling pathway.

Arsenic trioxide inhibits breast cancer cell growth via microRNA-328/hERG pathway in MCF-7 cells.

Arsenic trioxide (As2O3) has been widely used in the treatment of acute promyelocytic leukemia and has been observed to exhibit therapeutic effects in various types of solid tumor. In a previous study by this group, it was shown that As2O3 induces the apoptosis of MCF-7 breast cancer cells through inhibition of the human ether-à-go-go-related gene (hERG) channel. The present study was designed to further investigate the effect of As2O3 on breast cancer cells and to examine the mechanism underlying the regulation of hERG expression. The present study confirmed that As2O3 inhibited tumor growth in vivo, following MCF-7 cell implantation into nude mice. Using computational prediction , it was identified that microRNA (miR)-328 had a binding site in the 3'-untranslated region of hERG mRNA. A luciferase activity assay demonstrated that hERG is a target gene of miR-328. Further investigation using western blot analysis and reverse transcription-quantitative polymerase chain reaction revealed that As2O3 downregulated hERG expression via upregulation of miR-328 expression in MCF-7 cells. In conclusion, As2O3 was observed to inhibit breast cancer cell growth, at least in part, through the miR-328/hERG pathway.