4-Mercuric acetate estrone (4-MF1) is one of steroidal estrogens which have hi-her protective and therapeutic effects on dogs receiving 2.75 Gy of 60Co ?-ray iradiation.Among those experimental groups,the group treated with 4-ME1 15 mg i.m. two days before irradiation had the higest protective effect, all 5 dogs survived;The group treated with 4-ME 1 i.m. twice at 6,48 h after irradiation had the best therapeutic effect. The survival rate was elevated 54.4%(9/15), as compared with the control group.The clinical symptoms were milder, survival time of dead animals longer, and the WBC count higher.

ObjectiveTo observe the effect of vinpocetine sustained-release capsules on post-stroke depression and recovery of neurological function. MethodsA total of 64 patients with acute post-stroke depression were randomly divided into Vinpocetine sustained-release capsules group( 34 cases) and control group(30 cases). Conventional therapy was given to both groups. To the treatment group, vinpocetine sustained-release capsules was given at the same time. Depression status was assessed with Hamilton Rating Depression Scale(HAMD). Meanwhile ,Mimi-Mental State Examination( MMSE), National Institutes of Health Stroke Scale(NIHSS) and Activities of Daily Living(ADL)were given in to both groups. ResultsAfter 6 to 12 weeks' therapy, the total score of HAMD, NIHSS and ADL of Vinpoeetine group were significantly lower than the control group ( all P ＜ 0.05 ), MMSE score increased significantly ( P ＜ 0.05 ) in Vinpocetine group. The curative rate and effective rate of Vinpocetine group were 38％ and 91％. It was significantly higher than the 20％ and 73％ of the control group ( all P ＜ 0.05 ). ConclusionVinpocetine sustainedrelease capsules was effective to treat post-stroke depression. It could improve the emotional state of patients and promote the recovery of neurological function.

Objective To observe the effect of vinpocetine on monoamine transmitters in cerebral of poststroke depression (PSD)rats and to investigate the mechanism of pharmacotherapeutics on PSD. Methods Rats were divided randomly into the sham-operated group,the normal saline group,the low dose of vinpocetine group and the high dose of vinpocetine group. Giving the left middle cerebral artery occlusion, the PSD rat model was established by unexpected chronic mild stress. When the PSD rat model was established, vinpocetine group was given vinpocetine(5mg/kg, 10mg/kg) and the normal saline group was given normal saline. Then the ethological score of depression was evaluated on 14 and 28 days. The monoamine transmitter in the frontal cortex and hippocampus and brainstem were detected by the fluorospectrophotometry. Results On the 28th day after the model establishment,compared with the normal saline group, the ethological score of depression level was decreased obviously. Compared with the normal saline group, vinpocetine could improve the ethological score of depression level of the PSD rat model, and these concentrations of 5-hydoxytrypatarmine ( 5-HT), noradrenalin ( NE ) and dopamine ( DA ) in the frontal cortex, hippocampus and brainstem. The level of NE ( ( 192.4 ± 34.8 ) ng/g, ( 206. 0 ± 41.7 ) ng/g,(91.1 ±23.0) ng/g] ,5-HT( (494. 1 ± 50.7) ng/g, (599.7 ± 39.2) ng/g, (541.7 ± 62.6) ng/g) and DA ( ( 298.6 ± 32.6) ng/g, ( 297.0 ± 38.1 ) ng/g, ( 85.9 ± 24.3 ) ng/g) in the high dose of vinpocetine group were significantly higher than that in the normal saline group ( NE (92.4 ± 17.5 ) ng/g, ( 131.4 ± 34.8 ) ng/g, (49.0 ±13.6)ng/g;5-HT(367.8 ±87.3) ng/g,(498.7 ± 79.6) ng/g, (320.4 ±59.4) ng/g; DA( 106.1 ±23.0)ng/g,(97.0 ±21.7)ng/g, (50.4 ± 13.8 )ng/g)(P ＜ 0.01 ). There were increased obviously by the high dose than the low dose of vinpocetine group. Conclusion Vinpocetine could treat PSD by increasing the level of monoamine transmitters in PSD rats' brain.

The activity of colony stimulating factor ( CSF) in the conditioned medium ( CM ) was studied with combination method of 3H-TdR incorporation assay and agar colony assay. These two assays were demonstrated to be replaceable each other. The mice were administered with nontoxic monophosphoryl lipid A(MPLA) which was derived from a Re mutant of Salmonnella Minnesota Re595. The results showed a significant elevation of CSF in the serum and reaching the top at 12th h and returning to normal by 24th h. There is a significant dose-resoonse relationship. The CSF was induced with accompany of formation of colony inhibiting factor (GIF), some of which were heat sensitive factors. It is suggested that the MPLA may be a potent CSF-inducer.

Objective To evaluate the endotoxin-neutralizing activity of modeling peptides from the limulus antilipopolysaccharide factor (MPLALFs, Ms) in vitro. Methods The endotoxin-binding activity of Ms was examined by biosensor technique and shown in values of Kon and Kd. The endotoxin-neutralizing effect was analyzed by limulus amebocyte lysate test. Results The biosensor technique results showed that the Kon values of M_0, M_1, M_2, M_3, M_4, M_6, M_8 and M_ 10 binding to LPS 055∶B5 were (840?5.716), (549?6.532), (842?6.530), (627?2.450), (996?5.716), (814?8.982), (556?1.633) and (635?2.449) arc second, of which M_4 and M_1 had the highest and lowest endotoxin-binding activity, respectively. The M_4 reacted to LPS with a Kd of 72.377 ?mol/L. The results obtained by the limulus amebocyte lysate test were the same with those from the biosensor technique. Conclusion M_4 has a potential good endotoxin-neutralizing effect in vitro.

Objective:To analyze the effect of glucocorticoid on the biological function of lens epithelial cells (LECs) by bioinformatics and predict related microRNA (miRNA).Methods:GSE3040 database was downloaded and the human LECs line (HLE-B3) cells in the experimental group were treated with 1 μmol/L dexamethasone, and HLE-B3 cells in the control group were treated with 1 μmol/L dimethyl sulfoxide(DMSO).GEO2R was used to analyze the differentially expressed genes between the two groups.Metascape website was employed to analyze the functional enrichment of differentially expressed genes, and EdU cell proliferation assay was performed to detect the difference in cell proliferation between the two groups.STRING website and cytoscape software were used to construct protein-protein interaction network.Hub genes were calculated by cytohubba app, and quantitative real-time PCR was performed to detect the expression levels of hub genes between the two groups.MirCode website was used to predict the related miRNAs.Results:A total of 341 differentially expressed genes were detected between the experimental group and the control group, among which there were 300 up-regulated genes and 41 down-regulated genes. SLC12A1, MED13L, ALDH5A1, SLC15A3 and WWC1 were the top five down-regulated genes and SCNN1A, ANKRD36, FKBP5, PYY and ADH1B were the top five up-regulated genes.The top 20 terms of functional enrichment were listed, and the negative regulation of HLE-B3 cells proliferation showed the most enrichment.Cell proliferation rate in the experimental group was (8.09±0.20)%, which was significantly lower than (39.63±0.80)% in the control group ( t=38.43, P<0.01).The top ten hub genes were SST, CXCL8, GRM1, GNRH1, CXCL5, PPBP, CX3CR1, PYY, EDNRA and GRK5, and quantitative real time PCR confirmed that the expression levels of SST, CXCL8, GRM1, PYY, EDNRA and GRK5 mRNA were statistically different (all at P<0.05).The top six miRNAs which might be associated with hub genes were miR-15abc, miR-214, miR-23abc, miR-129-5p, miR-132 and miR-24. Conclusions:The 1 μmol/L glucocorticoid can negatively regulate the proliferation of HLE-B3 cells. SST, CXCL8, GRM1, PYY, EDNRA and GRK5 may be hub genes and miR-15abc, miR-214, miR-23abc, miR-129-5p, miR-132, miR-24 are most likely to relate to them.

Objective To investigate the effects of methamphetamine (Meth) on the outward K+ currents and elucidate the role of outward K+ channels in Meth induced hippocampal neuron damage.Methods Hippocampal neurons were harvest from 18-day-old embryonic rats and were divided into two groups:the control group and the Meth treated group.Both of 4-AP and TEA sensitive K+ currents were recorded after the treatment of Meth by performing the whole cell patch clamp.Furthermore,the MTT and TUNEL assays were performed to evaluate the effects of K+ channel on hippocampal neuron damage mediated by Meth.For statistical comparison,One-way ANOVA and LSD multiple comparison test or t-test was used.P-value ＜ 0.05 was considered to be statistically significant.Results The density of 4-AP sensitive K+ channel currents in Meth treated group [(120.1 ± 19.6) pA/pF,n =7] were significantly increased when compared with control group [(87.4 ± 12.5) pA/pF,n =10,P ＜0.01] and the increments of the currents induced by Meth was dose dependent.The MTT data showed that the cell viability was obviously decreased in Meth treated group (48.72 ± 4.38) ％ relative to the control group (100.07 ± 3.36) ％.Moreover,application of K+ channel antagonist,4-AP (61.39 ± 3.15)％,and the high K+ solution (78.25 ± 9.42) ％ substantially enhanced the cell viability.The TUNEL assay showed there were protective effects of 4-AP and the high K+ solution against neuron damage observed during cells exposed to Meth.Conclusions The increments of 4-AP sensitive K+ channel currents induced by Meth might be involved in hippocampal neuron damage.

Objective To observe the expression of small ubiquitin?related modifiers(SUMO)protein in normal cultured human lens epithelial cells(SRA01/04)and discuss regulation effects of SUMO protein on oxidative stress induced by high glucose. Methods The expression and local?ization of SUMO 1,2/3,4 was detected in normal cultured SRA01/04 cells through immunocytochemistry. The mRNA expression levels of SUMO 1?4 were examined by RT?PCR after the SRA01/04 cells treated with high glucose media at different concentrations and time points. Samples were grouped by medium concentrations(glucoses 5.5 mmol/L,12.5 mmol/L,25 mmol/L,50 mmol/L respectively for 24 h)and by treatment time(0 h, 6 h,12 h and 24 h respectively). After highly efficient transfection of GFP?SUMO2 into SRA01/04 cells,the survival and apoptotic rates of transfect?ed and un?transfected cells treated with high glucose was detected by CCK8 method and AV/PI double staining flow cytometry. Results The immu?nocytochemistry results showed that SUMO1,2/3,4 proteins were mainly located in the nucleus of SRA01/04 cells and part of SUMO2/3 was in the cytoplasm. RT?PCR results showed that compared with the low?glucose group,the mRNA expression of SUMO1?4 was increased along the increas?ing glucose concentration in the high?glucose group(P<0.05). Compared with 0 h,the mRNA expression of SUMO1?4 was enhanced at 6 h,12 h and 24 h(P<0.05)in the high?glucose group treated at 50 mmol/L concentration. Compared with the un?transfected cells,the survival rate was in?creased and the apoptotic rate was decreased in GFP?SUMO2 transfected cells in oxidative stress induced by high glucose(P<0.05). Conclusion SUMO protein was positively expressed in SRA01/04 cells and the expression of SUMO mRNA was affected by oxidative stress induced by high glu?cose.

AIM:To study the protection and mechanism of Asclepiadaceae against the damage of neuron by free radical. METHODS:The model of ischemia and damaged neuron induced by H 2O 2 was made respectively. The protection of Asclepiadaceae was observed with the measurement of contents of MDA in brain and cultured neuron, transudatory rate of LDH, breaking rate of DNA and clearance rate of?OH in cultured neuron. RESULTS:Asclepiadaceae decreased the raising of MDA in brain induced by ischemia. The raising of transudatory rate of LDH,breaking rate of DNA and content of MDA inducing by H 2O 2 in cultured neuron were also observed. The clearance rate of?OH in cultured neuron increased as the contents of Asclepiadaceae raised. CONCLUSION: The mechanism of Asclepiadaceae protecting the neuron is related to its ability to clean up free radical.

Objective To establish the ischemic precondition ([PC) model of PC12 cell line in vitro, and to explore the effect of nitric oxide (NO) on the IPC cerebral protection. Method PC12 cells were cultured and used for producing the model of ischemie precondition by the way of oxygen-glucose deprivation. Twenty dishes of cells were randomly divided into four groups (5 dishes for each group): control group, ischemic precondition group (IPC),non-ischemic precondition group (NIPC) and L-NAME treatment group (L-NAME). In control group, the cells were in-cubated with low glucose (<1 g/L) and2% FBS medium in normal oxygen; in IPC group, the cells were administrated with oxygen-glucose deprivation (OGD) for 6 hours, and then subjected with reperfuaion before OGD 15 hours; in NIPC group, the cells were treated the same as control group for 6 hours, and then subjected with reperfusion before OGD 15 hours; in L-NAME group, the cells received L-NAME (1 mmol/L) and cocultured for 30 minutes before OGD 6 hours, and then received the same treatment as the IPC group. To test whether the model was established, metabolic rate of MIT, LDH release were measured and the apoptosis rate was detected by flow cytometry following oxygen-glucose deprivation 15 hours. The activity of nitric oxide synthases (NOS) was as-sessed by biochemical assay. One-way ANOVA and LSD multiple comparison test were used to analyze differences among different groups, and P<0.05 was considered different. Results Compared with NIPC group, the metabolic rate of MTT increased (94.9%±35.1%, P<0.05), while LDH release and the cell apoptotic rate decreased significantly in IPC group (279.1%±28.1%, P<0.03). Compared with control group(100.0%± 13.5%),the activities of NOS increased both in NIPC and IPC groups (390.0%±14.6%, P<0.01;126.3% ±10.6%, P<0.01). Moreover, the apoptosis rates in each group (control group, IPC group, NIPC group and L-NAME group) were 5.90, 8.73, 38.62 and 11.73%,respectively. Conclusions IPC reduces the death and apoptosis rate of PC12 cell after oxygen-glucose deprivation injury. NO might be involved, but it is not the only factor.