RESUMEN
The purpose of this study is to investigate the effects of melatonin on the radiosensitivity of HeLa cells. Concentration from 10 to 1000 µM of melatonin was used on HeLa cells before X-rays irradiation (IR). The cellular inactivation effect was analyzed by clonogenic assay, and cell growth was measured by MTT assay at various concentrations. Ten micrometer melatonin promoted the cell-killing effects of IR, while 1000-µM melatonin prevented IR-induced cellular inactivation. Further analysis revealed that 1000-µM melatonin protected the cells from IR-induced reactive oxygen species damage, as the oxidative stress measured by fluorescent microscopy and fluorescence-activated cell sorting using 2,7-dichlorofluorescein diacetate staining. This is further confirmed by melatonin receptor agonist, which has no antioxidant capacity. A 10-µM melatonin, on the contrary, enhanced the cell-killing effects of IR by activating c-Jun NH2-terminal kinase (JNK) signaling. c-Jun NH2-terminal kinase signaling activation was indicated by Western blot of phosphorylated JNK. We used JNK inhibitor to further confirm the involvement of JNK signaling in the cell-killing enhancement of 10-µM melatonin administration. Our results suggest the importance of dose-dependent effects in melatonin application for radiotherapy.
RESUMEN
Magnetic resonance imaging (MRI) features of intracranial anaplastic hemangiopericytoma (AHPC) were analyzed. The pathological examination showed that there was a great number of irregularly arranged tumor cells with nuclear atypia, and mitotic properties were commonly seen providing support for clinical staging, therapy and prognosis judgment. Eighteen cases of intracranial AHPC proved by operation and pathology were analyzed retrospectively. Both plain and enhanced MR scans were performed and the results were compared with pathology in all cases. In all 18 cases, the tumor was positioned in the cortex; in 12 cases, it was located in the frontal falx and in 3 cases, it was located in the parietal falx. In 2 cases, the tumor was located in the middle cranial fossa, and in 1 case, it was located in the cerebellar hemispheres. Thirteen of the 18 cases showed mixed hyper-iso signal intensity with cortical grey matter, and the other 5 cases were isointense in the cortical grey matter on T1-weighted images. Fifteen of the 18 cases showed heterogeneous hyper-iso signal intensity, and the other 3 cases were isointense on T2-weighted images. Fifteen of the 18 cases showed heterogeneous enhancement in contrast-enhanced T1-weighted images. Our data show that, because intracranial AHPC has specific features on MRI, it could be very useful for its clinical diagnosis.