Objective To study the protective effect of galanin on 2,3-Dimethoxy-1,4-naphthoquinone (DMNQ)-induced oxidative stress and cell damage in HEK-293A cells and its possible mechanisms.Methods The expression of galanin and its three receptors (GalR1-3) in HEK-293A were determined with RTPCR technique.The cultured HEK-293A cells were divided into four groups:Control,DMNQ,DMNQ + GAL and DMNQ + AR-M1896 and the cell viability was measured with CellTiter 96 AQueous One Solution Cell Proliferation Assay (MTS).Results The RT-PCR data revealed the presence of galanin and its receptors in HEK-293A cells.The expression level was in the order of GalR2 =Galanin ＞ GalR3 ＞ GalR1.DMNQ caused oxidative stress and cell damage in HEK-293A cells with a dose-dependent manner with an IC50 =13.4 μM.Application of galanin reduced the DMNQ-induced cellular toxicity in HEK-293A,which increased cell viability by 24.4％ and 18.8％ in 1 μM and 100 nM,respectively.AR-M1896,an agonist of GalR2 had a similar effect,increased cell viability by 8.7％ and 8.9％ in 1 μM and 100 nM,respectively.Conclusion These data suggest that galanin has a protective effect on DMNQ-induced oxidative stress and cell damage in HEK-293A cells,probably mediated by GalR2.

Objective To investigate the expression of glutathione S-transferase π (Glutathione S-transferase π, GST-π) protein in peripheral blood and brain of patients with drug-resistant epilepsy and refractory epilepsy rats. Meth?ods From January 2010 to March 2014, the expression of GST-πin the blood and brain of 32 cases of drug-resistant epi?lepsy underwent neurosurgery and 10 cases of cerebral vascular malformation underwent surgery were studied and com?pared. The expression of GST-πin the blood and brain in refractory epilepsy rats and normal rats were studied and com?pared. Results The specimen from 20 temporal, 6 frontal and 6 occipital lobes were obtained from drug-resistant epilep?sy patients. The expression levels of GST-πin the blood and brain in refractory epilepsy rats and normal rats were higher than those of the control groups (P<0.05). Conclusion GST-πmay be involved in the process of drug-resistant epilepsy. The GST-πexpression in blood may be used as a marker for resistance to anti-epileptic agents.

Objective To investigate the changes of ANF mRNA expression in the myocardial tissues of rat embryo and neonate induced by 2,3,7,8-TCDD so as to determine if TCDD can cause injuries of cardiac functions. Methods SD rat embryos were divided into 4 groups respectively exposed to TCDD at the dose of 0.05,0.5,5,10 ?g/kg. The mRNA expression of ANF/ANP in the myocardial tissues of rat embryos of day 15,19 and suckling rats aged 5 days were detected by semiquantitative RTPCR analysis. Results TCDD could upregulate ANF mRNA expression in the myocardial tissues of rat embryos and suckling rats,as compared with control group. Conclusion TCDD can upregulate ANF mRNA expression in myocardial tissues,suggesting that TCDD may cause injuries of cardiac functions of rat embryos and suckling rats.

Objectives To prospectively investigate the diagnostic accuracy,image quality and radiation doses of prospectively ECG-triggered high-pitch spiral acquisition computed tomography coronary angiography (CTCA) using Flash dual-source CT for the diagnosis of significant coronary stenoses.Methods Seventy-three patients underwent both CTCA and CCA.CTCA was performed using a Flash dual-source CT system with data acquisition at a high-pitch of 3.4.CCA served as the standard of reference.Radiation dose values were calculated using the dose-length product.Results There were 925 vessel segments in 73 patients.(1)Diagnostic accuracy: the sensitivity,specificity and positive and negative predictive values were 93.2％ (164/176),96.4％ (722/749),85.9％ (164/191),98.4％ (722/734) for segment assessment and 98.4％ ( 123/125 ),87.4％ ( 83/95 ),91.1％ ( 123/135 ),97.6％ ( 83/85 ) for vessel assessment and 100％ (44/44),89.7％ ( 26/29 ),93.6％ ( 44/47 ),100％ ( 26/26 ) for patient assessment.( 2 ) Image quality: there were 2 coronary segments of right coronary artery and one segment of left circumflex artery with non-diagnostic image quality.There was no non-diagnostic image quality in left anterior descending artery.(3) Radiation dose: the effective radiation dose was ( 1.14 ± 0.10) mSv.Conclusions CTCA using the prospectively ECG-triggered high-pitch spiral mode of the Flash dual-source CT system is associated with high diagnostic accuracy for the assessment of coronary artery stenoses at low dose.

Objective To investigate the effect of statin therapy on pneumonia and stroke outcome after acute ischemic stroke.Methods The patients with pneumonia after acute ischemic stroke were enrolled retrospectively.The demographic and clinical data of the patients were collected,including whether using statins,the clinical features of pneumonia,the days of using antibiotics,and neutrophil count.They were divided into either a statin group or a control group according to whether they used statins or not.Stroke outcome was evaluated with the modified Rankin scale.Results A total of 53 patients with pneumonia after acute ischemic stroke were enrolled in the study,20 of them were in the statin group and 33 were in the control group.There were no significant differences in age and the proportions of male and complicated with hypertension,diabetes and coronary heart disease between the statin group and the control group (all P ＞ 0.05).The cure rate,improvement rate,invalid rate and mortality in the statin group were 50.00％,35.00％,15.00％ and 0.00％,respectively; and in the control group were 15.15％,39.40％,33.30％ and 15.15％,respectively.There were significant differences (P =0.003).The days of temperature returning to normal (2.10 ± 3.29 d vs.4.61 ±3.54 d; P =0.002),pulmonary rales disappearing (3.60 ±2.46 d vs.7.67 ±4.09 d; t =-4.019,P =0.000)and using antibiotics (7.05 ± 3.13 d vs.9.73 ± 4.00 d; t =-2.562,P =0.013) in the statin group were significantly shorter than those in the control group,while there were no significant differences in the days of cough and sputum production retuming to normal between the 2 groups.The proportions of diabetes (20.83％ vs.55.17％ ;x2 =6.473,P =0.011),posterior circulation stroke (4.7％ vs.27.59％ ; P =0.031)and bilateral lung shadows (29.17％ vs.55.17％ ;x2 =5.705,P=0.017),as well as baseline National Stroke Association NIH Stroke Scale (NIHSS) score (4.00 ± 4.54 vs.10.66 ± 6.33; t =1.898,P =0.001) in a good outcome group were significantly lower than those in a poor outcome group.But there was no significant difference in the proportion of the patients treated with statins between the good outcome group and the poor outcome group (41.67％ vs.34.48％ ;x2 =0.288,P =0.591).Multivariate logistic regression analysis showed that diabetes (odds ratio [OR] 5.146,95％ confidence interval [CI] 1.166-22.709; P =0.031) and baseline NIHSS score (OR 1.251,95％ CI 1.080-1.449; P =0.003) were the independent risk factor for patient with poor outcomes.Conclusions Statins may promote the pneumonia recovery in patients with acute ischemic stroke; however,it has no effect on stroke outcome.

Objective To evaluate the effects of baijin capsule on behavioral changes and monoamine neurotransmitters concentration in chronic unpredictable mild stress ( CUMS ) depression rat model.Methods The depression rat model was induced by11-week chronic unpredictable mild stress combining with solitary.After the model were established, rats were given the decoction of baijin capsule ( 12.6 g/kg, 4.2 g/kg, 1.4 g/kg ) or fluoxetine hydrochloride (3.5 mg/kg) by intragastricfor 4 weeks.During the experiment period, sucrose consumption and open-field experiment were conducted to monitor the behavior of rats, such as sucrose consumption percentage, horizontal motion, and vertical motion.At the end of the experiment, the levels of the monoamine neurotransmitters in the cerebral cortex and hippocampus were analyzed by method of high performance liquid chromatography-electrochemistry.Results Compared with the normal group, the weight, horizontal displacement distance, vertical movement times, and sucrose consumption percentage of rats in model group decreased significantly after stimulated with CUMS and solitary for 7 weeks (P<0.05,P<0.01).Compared with model group, consecutively administrated for 4 weeks, horizontal displacement distance, vertical movement times, and the percentage in sugar water consumption significantly increased with the treatment of baijin capsule (P<0.05, P<0.01).Meanwhile, the content of norepinephrine (NE), dopamine (DA), and 5-hydroxytryptamine (5-HT) in the cortex were significantly increased in rats of the baijin capsule ( P <0.05 ) .Conclusions The results indicated that baijin capsule improved the behavioral disturbances in depression rat model, which were related to enhancement of the concentration of monoamine neurotransmitters in the cortex.

Purpose: Temozolomide is used in first-line treatment for glioblastoma. However, chemoresistance to temozolomide is common in glioma patients. In addition, mechanisms for the anti-tumor effects of temozolomide are largely unknown. Ferroptosis is a form of programmed cell death triggered by disturbed redox homeostasis, overloaded iron, and increased lipid peroxidation. The present study was performed to elucidate the involvement of ferroptosis in the anti-tumor mechanisms of temozolomide. Materials and Methods: We utilized the CCK8 assay to evaluate cytotoxicity. Levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), iron, and glutathione (GSH) were measured. Flow cytometry and fluorescence microscope were used to detect the production of reactive oxygen species (ROS). Western blotting, RT-PCR and siRNA transfection were used to investigate molecular mechanisms. Results: Temozolomide increased the levels of LDH, MDA, and iron and reduced GSH levels in TG905 cells. Furthermore, we found that ROS levels and DMT1 expression were elevated in TG905 cells treated with temozolomide and were accompanied by a decrease in the expression of glutathione peroxidase 4, indicating an iron-dependent cell death, ferroptosis. Our results also showed that temozolomide-induced ferroptosis is associated with regulation of the Nrf2/HO-1 pathway. Conversely, DMT1 knockdown by siRNA evidently blocked temozolomide-induced ferroptosis in TG905 cells. Conclusion Taken together, our findings indicate that temozolomide may suppress cell growth partly by inducing ferroptosis by targeting DMT1 expression in glioblastoma cells.

Purpose: Temozolomide is used in first-line treatment for glioblastoma. However, chemoresistance to temozolomide is common in glioma patients. In addition, mechanisms for the anti-tumor effects of temozolomide are largely unknown. Ferroptosis is a form of programmed cell death triggered by disturbed redox homeostasis, overloaded iron, and increased lipid peroxidation. The present study was performed to elucidate the involvement of ferroptosis in the anti-tumor mechanisms of temozolomide. Materials and Methods: We utilized the CCK8 assay to evaluate cytotoxicity. Levels of lactate dehydrogenase (LDH), malondialdehyde (MDA), iron, and glutathione (GSH) were measured. Flow cytometry and fluorescence microscope were used to detect the production of reactive oxygen species (ROS). Western blotting, RT-PCR and siRNA transfection were used to investigate molecular mechanisms. Results: Temozolomide increased the levels of LDH, MDA, and iron and reduced GSH levels in TG905 cells. Furthermore, we found that ROS levels and DMT1 expression were elevated in TG905 cells treated with temozolomide and were accompanied by a decrease in the expression of glutathione peroxidase 4, indicating an iron-dependent cell death, ferroptosis. Our results also showed that temozolomide-induced ferroptosis is associated with regulation of the Nrf2/HO-1 pathway. Conversely, DMT1 knockdown by siRNA evidently blocked temozolomide-induced ferroptosis in TG905 cells. Conclusion Taken together, our findings indicate that temozolomide may suppress cell growth partly by inducing ferroptosis by targeting DMT1 expression in glioblastoma cells.

Objective:To explore the role and mechanism of Talin-1 in mouse aortic dissection.Methods:Sixty male FVB mice were evenly divided into groups of blank, model, Talin-1 up-regulation, Talin-1 up-regulation control, Talin-1 down-regulation, and Talin-1 down-regulation control. Except mice in the blank group, mice were treated with β-aminopropionitrile (BAPN) combined with angiotensin to construct a mouse aortic dissection model. Hematoxylin-eosin and vascular elastic fiber staining (EVG) were used to observe the aorta and elastic fiber morphology and structure. Western blot was used to detect the phosphorylation levels of FAK and ERK1 / 2 in mouse aortic tissue.Results:The success rate of aortic dissection in model mice was 70%, and there was no aortic dissection appeared in the blank group.No mice died during the experiment. The incidence of aortic dissection in the Talin-1 down-regulated group was 100%, which was significantly higher than that in the Talin-1 down-regulated control group( P<0.05). The incidence of aortic dissection in the Talin-1 up-regulated group was 20%, significantly lower than that in the Talin-1 up-regulated control group. The wall thickness of the aorta of mice in the Talin-1 down-regulated group was accompanied by hematoma or pseudocavity formation. The median elastic fiber content was higher than that in the Talin-1 downregulation control group( P<0.05). The content of elastic fibers in the blood vessel wall of mice in the Talin-1 up-regulation group was significantly higher than that in the Talin-1 up-regulation control group.The down-regulation of Talin-1 significantly inhibited FAK phosphorylation, and instead promoted ERK1/2 phosphorylation( P<0.05). Conclusions:Down-regulation of Talin-1 may reduce the elastic fiber content in the aorta of mice by activating the ERK1/2 signaling pathway, leading to vascular remodeling of the aortic wall and promoting the occurrence of aortic dissection.

OBJECTIVE： To prepare etoposide－ bovine serum albumin－ microspheres (VP－ BSA－ MS)and to study the distribution and pharmacokinetics of VP－ BSA－ MS in mice. METHODS: The drug concentrations in various tissues were determined by high－ performance liquid chromatograph (HPLC). RESULTS: The VP－ BSA－ MS was injected into mice and (47.88± 2.56 )％ of the total dosage was detected in lung tissue 15min after administration， the pharmacokinetical equation was C=149.0 897e－ 1.7 780t＋ 3.9 627e－ 0.0 398t — 153.0 524e－ 3.5 054t. CONCLUSION： The VP－ BSA－ MS showed remakable targeting action to the lung and the pharmacokinetic regularity could be discribed as two－ compartment model