Morin induces autophagy and apoptosis in hepatocellular carcinoma cells through Akt/mTOR/STAT3 pathway / 中国中药杂志

This study investigated the effect and mechanism of morin in inducing autophagy and apoptosis in hepatocellular carcinoma cells through the protein kinase B(Akt)/mammalian target of rapamycin(mTOR)/signal transducer and activator of transcription protein 3(STAT3) pathway. Human hepatocellular carcinoma SK-HEP-1 cells were stimulated with different concentrations of morin(0, 50, 100, 125, 200, and 250 μmol·L~(-1)). The effect of morin on the viability of SK-HEP-1 cells was detected by Cell Counting Kit-8(CCK-8). The effect of morin on the proliferation and apoptosis of SK-HEP-1 cells was investigated using colony formation assay, flow cytometry, and BeyoClick~(TM) EdU-488 with different concentrations of morin(0, 125, and 250 μmol·L~(-1)). The changes in the autophagy level of cells treated with morin were examined by transmission electron microscopy and autophagy inhibitors. The impact of morin on the expression levels of proteins related to the Akt/mTOR/STAT3 pathway was verified by Western blot. Compared with the control group, the morin groups showed decreased viability of SK-HEP-1 cells in a time-and concentration-dependent manner, increased number of apoptotic cells, up-regulated expression level of apoptosis marker PARP, up-regulated phosphorylation level of apoptosis-regulating protein H2AX, decreased number of positive cells and the colony formation rate, an upward trend of expression levels of autophagy-related proteins LC3-Ⅱ, Atg5, and Atg7, and decreased phosphorylation levels of Akt, mTOR, and STAT3. These results suggest that morin can promote apoptosis, inhibit proliferation, and induce autophagy in hepatocellular carcinoma cells, and its mechanism of action may be related to the Akt/mTOR/STAT3 pathway.

Inhibitory effect and molecular mechanism of sinomenine on human hepatocellular carcinoma HepG2 and SK-HEP-1 cells / 中国中药杂志

This study aimed to investigate the effect and molecular mechanism of sinomenine on proliferation, apoptosis, metastasis, and combination with inhibitors in human hepatocellular carcinoma HepG2 cells and SK-HEP-1 cells. The effect of sinomenine on the growth ability of HepG2 and SK-HEP-1 cells were investigated by CCK-8 assay, colony formation assay, and BeyoClick~(TM) EdU-488 staining. The effect of sinomenine on DNA damage was detected by immunofluorescence assay, and the effect of sinomenine on apoptosis of human hepatocellular carcinoma cells was clarified by Hoechst 33258 staining and CellEvent~(TM) Cystein-3/7Green ReadyProbes~(TM) reagent assay. Cell invasion assay and 3D tumor cell spheroid invasion assay were performed to investigate the effect of sinomenine on the invasion ability of human hepatocellular carcinoma cells in vitro. The effect of sinomenine on the regulation of protein expression related to the protein kinase B(Akt)/mammalian target of rapamycin(mTOR)/signal transducer and activator of transcription 3(STAT3) signaling pathway in HepG2 and SK-HEP-1 cells was examined by Western blot. Molecular docking was used to evaluate the strength of affinity of sinomenine to the target cysteinyl aspartate specific proteinase-3(caspase-3) and STAT3, and combined with CCK-8 assay to detect the changes in cell viability after combination with STAT3 inhibitor JSI-124 in combination with CCK-8 assay. The results showed that sinomenine could significantly reduce the cell viability of human hepatocellular carcinoma cells in a concentration-and time-dependent manner, significantly inhibit the clonogenic ability of human hepatocellular carcinoma cells, and weaken the invasive ability of human hepatocellular carcinoma cells in vitro. In addition, sinomenine could up-regulate the cleaved level of poly ADP-ribose polymerase(PARP), a marker of apoptosis, and down-regulate the protein levels of p-Akt, p-mTOR, and p-STAT3 in human hepatocellular carcinoma cells. Molecular docking results showed that sinomenine had good affinity with the targets caspase-3 and STAT3, and the sensitivity of sinomenine to hepatocellular carcinoma cells was diminished after STAT3 was inhibited. Therefore, sinomenine can inhibit the proliferation and invasion of human hepatocellular carcinoma cells and induce apoptosis, and the mechanism may be attributed to the activation of caspase-3 signaling and inhibition of the Akt/mTOR/STAT3 pathway. This study can provide a new reference for the in-depth research and clinical application of sinomenine and is of great significance to further promote the scientific development and utilization of sinomenine.

Bacteriological examination of digital X-ray imaging device before and after disinfection / 中华全科医师杂志

The digital X-ray imaging device was disinfected with trichloro-isocyanuric acid solution.The samples were taken with cotton swab pouring method before and 1,2,3 and 6 h after disinfection and the bacteriological examination was performed.Before disinfection the colony count of samples was all above the standard (＞ 10 cfu/cm2) with bacilli and gram-positive cocci predominantly.The highest count was detected in the X-ray photographic bed (58 cfu/cm2) and the lowest was in the exposure button(19 cfu/cm2).After disinfection the colony count in radiation suits still exceeded the standard,the colony count in diagnosis bed 2 h after disinfection,that in all parts of device 3 h after disinfection was off levels.The results indicate that the chlorine disinfectants can only achieve short-term effect in disinfection of digital X-ray imaging device.

Cognitive deficits in patients with brain tumor / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>To discuss the present status and progress of clinical research on the cognitive effects caused by different types of brain tumors and common treatments.</p><p><b>DATA SOURCES</b>The data used in this review were mainly from PubMed articles published in English from 1990 to Febuary 2012. Research terms were "cognitive deficits" or "cognitive dysfunction".</p><p><b>STUDY SELECTION</b>Articals including any information about brain tumor related cognitive deficits were selected.</p><p><b>RESULTS</b>It is widely accepted that brain tumors and related treatments can impair cognitive function across many domains, and can impact on patients' quality of life. Tumor localization, lateralization, surgery, drugs, radiotherapy and chemotherapy are all thought to be important factors in this process. However, some conflicting findings regarding brain tumor-related cognitive deficits have been reported. It can be difficult to determine the mechanism of these treatments, such as chemotherapy, antibiotics, antiepileptics, and steroids. Future research is needed to clarify these potential treatment effects.</p><p><b>CONCLUSIONS</b>Cognitive function is important for patients with brain tumor. Much more focus has been paid on this field. It should be regarded as an important prognostic index for the patients with brain tumor, and neuropsychological tests should be used in regular examinations.</p>

Frontal intraparenchymal schwannoma

A 39-year-old female had been subject to headache, and intermittent seizures for 9 years and decreasing memory for one year, without obvious neurological signs. An MRI revealed a 2x2 cm contrast-enhanced Wiaa in the frontal lobe, with a cyst and peritumoral edema, which was not attached to the dura or falx. Preoperatively, it was diagnosed as a glioma. Total surgical removal of the lesion led to a favorable result. Post-operative histo-pathological examination showed characteristic Antoni A and B areas consistent with intraparenchymal schwannoma. Intraparenchymal schwannoma is an extremely uncommon lesion, which is seen mostly in young adults and children. The main clinical symptoms include rising-intracranial-pressure-related manifestations and associated seizure disorders. The possible developmental origins, histological, imaging features, and protocols of treatment for this entity are discussed