Objective:To investigate the inhibitory effect of adenovirus-mediated recombinant Buthus martensii Karsch chloride toxin artifact (Ad-rBmK CTa) on human glioma U251 cells and its related mechanisms.Methods:Groups of 3 titer gradients of 3.5×10 9, 7.0×10 9 and 3.5×10 10 pfu/ml Ad-rBmK CTa were set up and applied to U251 cells for 24, 48 and 72 h, and a blank control group (no cells and Ad-rBmK CTa were added) and a negative control group (only U251 cells were added) were set up at the same time. The virus infection status was observed by laser confocal fluorescence microscopy. The cell proliferation in each group was detected by methyl thiazolyl tetrazolium (MTT) assay. The cell cycle and apoptosis in each group were detected by flow cytometry. The expressions of apoptosis-related proteins bax, bcl-2 and caspase-3 were detected by Western blot. Results:The infection rate of Ad-rBmK CTa was over 90% after acting on U251 cells for 24 h. As the titer of Ad-rBmK CTa increased, the proliferation inhibition rate of U251 cells treated for the same hours gradually increased (all P <0.01); with the extension of time, the proliferation inhibition rate of U251 cells treated with the same titer of Ad-rBmK CTa also gradually increased (all P < 0.01). After 7.0×10 9 pfu/ml Ad-rBmK CTa acted on U251 cells for 48 h, the proportion of cells in G 0/G 1 phase was (40.7±0.8)%, and cells in S phase and G 2 phase accounted for (35.7±0.6)% and (23.6±1.4)%, and the difference was statistically significant ( F = 225.119, P < 0.01). When 7.0×10 9 pfu/ml Ad-rBmK CTa acted on U251 cells for 24, 48 and 72 h, the apoptosis rates were (7.4±1.4)%, (19.2±1.7)% and (22.3±1.7)% ( F = 49.470, P < 0.01). After 7.0×10 9 pfu/ml Ad-rBmK CTa acted on U251 cells for 48 h, compared with the negative control group, the expressions of bax and caspase-3 proteins increased, and the expressions of bcl-2 decreased. Conclusions:Ad-rBmK CTa may act on the DNA damage-induced G 1/S detection site to arrest the cell cycle in G 0/G 1 phase, thus inhibiting the proliferation of U251 cells in vitro. However, its induction of apoptosis in U251 cells is not obvious. The mechanism may be related to the direct or indirect inhibition of chloride ion channels.

Glioma is a common tumor of the nervous system.In some gliomas, some of the expressions of microRNA are up-regulated.Some of them are down regulated.Some microRNA expressions promote the development of gliomas, while some microRNA exert inhibitory effects.MicroRNA is a small species, which is quite conservative in the evolution of species.It degrades messenger RNA or impedes its translation by guiding the silencing complex with target gene messenger RNA base pairs.Therefore, by studying the expression of microRNA in glioma, we can not only provide evidence for early diagnosis of glioma, but also provide a new plan for clinical treatment of glioma.By reading the literature, the expression of microRNA in glioma, the target of action and its effect on the biological characteristics of glioma were reviewed.

OBJECTIVE： To evaluate the efficacy and safety of progesterone in the treatment of acute traumatic brain injury systematically， and to provide reference for clinical use. METHODS： Retrieved from Cochrane library， ClinicalTrials， Web of Science， PubMed， Embase， CBM， CNKI and Wanfang database， randomized controlled trial （RCTs） about progesterone （trial group） versus placebo or blank control （control group） in the treatment of acute traumatic brain injury were collected. After literature screening， data extraction and quality evaluation by risk bias evalution tool of Cochrane systematic evaluator manual 5.1.0， Meta-analysis was performed by using Rev Man 5.3 statistical software. RESULTS： A total of 10 RCTs were included， involving 2 652 patients. Results of Meta-analysis showed that there was no statistical significance in mortality[RR＝0.77，95％CI（0.56，1.07），P＝0.12]， the incidence of septicemia [RR＝1.11，95％CI（0.77，1.60），P＝0.59] or elevated liver enzymes[RR＝1.30，95％CI（0.68，2.50），P＝0.43]. The number of patients with favorable neurological outcome[RR＝1.23，95％CI（1.05，1.43），P＝0.008] in trial group was significantly more than control group. Results of subgroup analysis of mortality showed that there was no statistical significance in the mortality of patient’s GCS≤8 [RR＝0.79，95％CI（0.57，1.10），P＝0.16]， that of patient’s GCS≤12[RR＝0.69，95％CI（0.23，2.10），P＝0.52] or that of patient’s GCS ranging from 9 to 12 [RR＝0.78，95％CI（0.26，2.35），P＝0.65] between 2 groups. Results of subgroup analysis of neurological outcome showed that there was no statistical significance in the number of favorable neurological outcome of patient’s GCS≤8 [RR＝1.18， 95％CI（0.98，1.43），P＝0.09]， the number of favorable outcome of patient’s GCS≤12[RR＝1.15，95％CI（0.87，1.51），P＝0.32] and the number of favorable neurological outcome of patient’s GCS ranging from 9 to 12[RR＝2.07，95％CI（0.24，17.71），P＝0.51]. CONCLUSIONS： Progesterone can improve the prognosis of neurological function in patients with acute traumatic brain injury with good safety but cannot reduce mortality.