Obesity increases the risk of ovarian cancer,and it is associated with the poor prognosis of ovarian cancer.Its pathogenic mechanism may be associated with the increased level of serum estrogen,insulin and insulin-like growth factors-1 induced by obesity and a variety of adipocytokines,which has an impact on the therapeutic result and prognosis of ovarian cancer.Maintaining a proper weight may prevent the development of ovarian cancer.

Objective The impact of complement Clq on inflammation in beta amyloidstimulated microglia.Methods After the cultured BV-2 microglial cells were treated with 100mg/L beta-amyloid fibers (fAβs),some of them were given C1q,others wcrc given C1q and C1qA.Then,interleukin-6 (IL-6) and tumor necrosis factor α (TNF α) in the supernatant and cell lysate were determined by the sandwich ELISA.Results A significant increase in TNF-α started at giving 50 nmol/L C1q after 100 mg/L fAβs (F =1177.27,P＜ 0.05),while the release of TNF-α was significantly suppressed by using 50 nmol/L C1qA on basis of this(P＜0.05).The level of IL-6 showed no above change.Conclusions C1q may enhance the inflammation of Aβ-induced BV-2 microglia cells and TNF-α may play important role in this effect.

Objective To observe the effect of suramin combinated with PG-Rg3 on xenograft growth of lung adeno-carcinoma in mice, and the related mechanism thereof. Methods Forty C57BL/6J mice bearing Lewis cells were random-ized into five groups:control group, cisplatin (DDP) group, suramin group, PG-Rg3 group and combination group. Appropri-ate interventions were given in five groups of mice. Mice were sacrificed at day 24 after tumor inoculation. The subcutaneous tumors were stripped for histological examination. The tumor inhibitory rate was measured. The expressions of erythropoietin-producing hepatoma amplified sequences (Eph) B4 protein, Bcl-2 and tumors microvessel density (MVD) were determined by immunohistochemistry method with image analyze system. The apoptosis of tumor cells was measured by biotinyated dUTP nick and labeling (TUNEL) method. Results There were significantly lower values in subcutaneous tumor volume and weight in drug-treated groups than those in control group (P<0.05). The inhibitory rates were 39.20%, 49.11%, 54.86%and 62.49%in cisplatin group, suramin group, PG-Rg3 group and combined group (P<0.05). The values of EphB4, MVD and Bcl-2 grey values were significantly decreased, the apoptotic index was significantly increased, in suramin group, PG-Rg3 group and combined group than those of control group and DDP group (P<0.05). The values of EphB4, MVD and Bcl-2 grey values were significantly increased, the apoptotic index was significantly decreased, in suramin group and PG-Rg 3 group than those of combined group (P<0.05). Conclusion Suramin combinated with PG-Rg3 can produce a synergetic inhibitory activity against tumor growth of lung adenocarcinoma, which may be associated with the effect of suppressing the expression of EphB4 and angiogenesis, and the promotion of tumor cell apoptosis.

Objective To observe the anti-tumor effects of Agrimonia Pilosa Ledeb(APL) ,a Chinese herbal medicine ,on hepato-cellular carcinoma cells in vitro and investigate the underlined mechanisms preliminarily .Methods APL water extracts were pre-pared .SMMC-7721 cells were cultured with the medium containing different concentrations of APL water extracts ,and at different time points ,cell viabilities were measured by the MTT assay and inhibitory rates (IR) were calculated ;cell morphologic changes were observed under a light microscope ;apoptotic ratios were measured by flow cytometry ;and the expressions of Bcl-2 and P53 proteins were examined by immunocytochemistry .Results After the cells were cultured with the medium containing APL water ex-tracts for 24 h ,48 h and 72 h ,no obvious effects were found on the cell proliferation in 5 mg/mL group and 10 mg/mL group ,but IR were 0 .5% ,23 .9% and 27 .5% in 20 mg/mL group and 23 .3% ,51 .7% and 71 .6% in the 40 mg/mL group ,respectively .In the groups with effects on the cells proliferation ,morphological characteristics of apoptosis were obvious ,and the cell apoptotic ratios were 19 .5% and 23 .0% in 20 mg/mL group and 33 .4% and 42 .7% in 40 mg/mL group at 48 h and 72 h .The expressions of Bcl-2 protein were 71 .9% and 58 .5% in 20 mg/mL group and 47 .9% and 26 .5% in 40 mg/mL group at 48 h and 72 h ,and the ex-pressions of P53 protein were 22 .9% and 50 .6% in 20 mg/mL group and 48 .7% and 83 .7% in 40 mg/mL group at 48 h and 72 h . Conclusion The water extracts of APL are able to inhibit proliferation and induce apoptosis of SMMC-7721 cells dose-time depend-ently in vitro ,which might be associated with the expression changes of Bcl-2 and P53 protein .

Objective To study the effects of butylphthalide (NBP) on memory and apoptosis related protein as well as neuronal pathology in hippocampus of vascular dementia (VD) rats. Methods VD model was generated by the permanent occlusion of bilateral common carotid arteries in SD rats to produce the forebran ischemia. Male SD rats were randomly allocated into sham-operation group, VD model group, NBP treatment group and nimodipine treatment group. The function of memory was tested by the Morris water maze. The neuronal pathological changes and the expression of Bcl-2 and Bax proteins in the hippocampus were observed with hematoxylin-eosin (HE) staining and immunohistochemical staining, respectively. Results The impaired memory of VD rats was proved by the lengthened mean escape latency [(78.79±21.93)vs.(16.96±7.44),P＜0.05] and the neuron in hippocampus was severely damaged. The decveased ratio of Bcl-2/Bax resulted from the overexpression of Bax proteins in VD model group versus the sham-operation group [(43.00±6.72)vs.(6.00±1.29),P＜0.05]. The treatment of NBP notably improved the memory function of VD rats and reduced the hippocampus pathological injury (P＜0.05). The expression of Bcl-2 protein raised [(33.14±8.05)vs.(21.81±4.97),P＜0.05] along with reduced expression of Bax protein [(32.93±4.99)vs.(43.00±6.72),P＜0.05] after NBP treatment. However, there was no significant difference in the treatment effects between nimodipine and NBP group (P＞0.05). Conclusions NBP treatment could improve memory of VD rats and reduce the hippocampus pathological lesion by inhibiting the apoptosis related protein.

Objective To investigate the neuroprotective effect and its mechanism of p38 mitogenactivated protein kinase inhibitor after subarachnoid hemorrhage (SAH).Methods Twenty-seven SPF-grade adult male SD rats were selected to induce a SAH model using the prechiasmal pool blood injection.Three dead rats were excluded.Twenty-four rats were randomly divided into four groups:sham operation group,SAH group,dimethyl sulfoxide (DMSO) group,and DMSO +p38 inhibitor group (n =6 in each group).Western blot was used to detect the expression levels of p38,phosphorylation p38,Parkinson's disease protein 7 (DJ-1),autophagy associated gene 5 (Atg5),autophagy adaptor protein p62,microtubule-associated protein Ⅰ Light Chain 3 (LC3-Ⅰ),microtubule-associated protein Ⅱ light chain 3 Ⅱ (LC3-Ⅱ),and the Garcia neurological function score was used to judge the nerve injury.PC12 cell oxygenated hemoglobin was used to induce an in vitro SAH model.They were completely randomly divided into four groups:sham operative group,SAH group,DMSO group,and DMSO + p38 inhibitor group.Fluorescent probe JC-1 was used to observe the changes of mitochondrial membrane potential.Results (1) There were significant differences in the expression of p38,phosphorylation-p38 and DJ-1 in rat brain tissue among the 4 groups (F values were 94.959,150.293 and 698.476,respectively,all P ＜ 0.01).There were significant differences in mitochondrial membrane potential in PC12 cells among the 4 groups (F value was 24.989,P ＜ 0.01).There were significant differences in the expression levels of autophagy related protein LC3-Ⅱ/LC3-Ⅰ ratio,Atg5 and p62 in rat brain tissue among the 4 groups (F values were 235.319,110.490 and 36.311,respectively,all P ＜ 0.01).There was significant difference in nerve function score among the 4 groups (F value was 25.550,P ＜ 0.01).(2) Compared with the sham operative group,the expression levels of p38,phosphorylation-p38 and DJ-1 were upregulated significantly after SAH (from 0.43 ±0.06,0.41 ±0.02 and 0.07 ±0.01 to 0.61 ± 0.08,0.79 ± 0.07 and 0.17 ± 0.03,respectively,all P ＜ 0.01),mitochondria membrane potential depolarization (from 8.29 ±0.28 to 9.23 ±0.42,P ＜0.01);upregulation of Atg5 expression and increase of LC3-Ⅱ/LC3-Ⅰratio (from 0.23 ± 0.04 and 0.25 ± 0.04 to 0.47 ± 0.04 and 0.46 ± 0.04,respectively,all P ＜ 0.01),down regulation of p62 expression (from 1.09 ± 0.14 to 0.54 ± 0.10,P ＜ 0.01);neurological score was decreased (from 17.5 ± 0.6 to 11.3 ± 2.7,P ＜ 0.01);p38 inhibitor was significantly down regulated the expression of phosphorylation-p38 after SAH (from 0.79 ± 0.07 to 0.47 ± 0.04,P ＜ 0.01),the expression of DJ-1 was up-regulated (from 0.17 ± 0.03 to 1.02 ± 0.06,P ＜ 0.01),mitochondrial membrane potential recovery (from 9.23 ±0.42 to 8.47 ±0.36,P ＜0.01),cell autophagy related protein LC3-Ⅱ/LC3-Ⅰ ratio and Atg5 were upregulated(from 0.46 ±0.04 and 0.47 ±0.04 to 0.77 ± 0.06 and 0.95 ± 0.12,all P ＜ 0.01),p62 expression returned to the levels of SAH group (from 0.57 ± 0.09,to 0.54 ± 0.10,P =0.650),and the neurological score was significantly improved (from 11.3 ± 2.7 to 15.5 ± 1.0,P ＜0.01).Conclusions After SAH,the p38 inhibitor downregulates the activity of2 phosphorylation p38.It may inhibit abnormal autophagy and maintain mitochondrial function by up-regulating the expression of DJ-1 protein,and then play a neuroprotective function.

Objective:To evaluate association of peripheral blood brain-derived neurotrophic factor (BDNF) with Alzheimer's disease (AD) .Methods:Databases including Pubmed, Cochrane library, Web of science, Embase, China National Knowledge Infrastructure, CBM disc, VIP-CSTJ and Wanfang Data were used to collect case-control studies related to the concentration of BDNF in peripheral blood of dementia patients with Alzheimer's type(DAT) and mild cognitive impairment(MCI). After extracting data and appraising the quality of the included studies, meta-analysis were conducted using Review Manager 5.3 and CMA 3.0.Results:A total of 51 articles were included in the analysis, with a total subjects of 7 182, including 2 673 subjects in DAT group, 1 506 subjects in MCI group, and 3 003 subjects in control group.The Meta-analysis showed that the levels of peripheral blood BDNF in patients with DAT were significantly lower than normal control group(SMD=-0.71, 95% CI : -0.99--0.43, P<0.001) ( n=5 111), and there were no statistical differences in peripheral blood BDNF levels between MCI group and control group and between DAT group and MCI group.The subgroup analysis showed that the level of serum BDNF in patients with DAT (SMD=-0.85, 95% CI: -1.15--0.55, P<0.001)( n=4 425) and MCI(SMD=-0.38, 95% CI: -0.62--0.14, P=0.002)( n=2 476) was significantly lower than that in normal control group, and the level of serum BDNF (SMD=-0.76, 95% CI: -1.37--0.16), P=0.01)( n=1 630) in patients with DAT was lower than that in MCI; However, there were no statistical difference among DAT, MCI and control groups in the level of plasma BDNF( P>0.05). Conclusion:The patients with DAT and mild cognitive impairment have lower level of serum BDNF, which suggesting that serum BDNF level may be a potential biomarker for early diagnosis of AD.

ObjectiveTo explore a feasible animal model of dysphagia after stroke. MethodsTwenty-two clean Sprague-Dawley rats were randomly divided into normal group (n = 11) and model group (n = 11). The model of dysphagia after stroke was established by the thread embolism, and the normal group received no intervention. The latency of the first swallowing attack and the number of swallowing were recorded three and seven days after modeling. The cerebral infarction was detected by TTC staining, and the neuronal apoptosis in ischemic brain was detected by TUNEL fluorescence staining. ResultsCompared with the normal group, the swallowing latency prolonged and the number of swallowing reduced three days in the model group, however, there was no significant difference (P > 0.05); seven days after modeling, the swallowing latency prolonged (P < 0.05), and the number of swallowing slightly reduced with little significant difference (P > 0.05). Compared with the normal group, the brain tissue showed obvious infarction area and a large number of apoptotic cells, while the body mass reduced in the model group (P < 0.05). ConclusionThe model rats express some features of dysphagia, which may become a transformation model of dysphagia after stroke.