Wheat bran, as the testa of wheat, has a long history of medication. Modern studies have discovered that wheat bran contains dietary fiber, phenolic compounds, proteins, vitamins, minerals and many other compounds, and boasts wide pharmacological activities such as blood glucose reduction, hypertension reduction, lipid reduction, anti-oxidation, anti-bacteria, anti-inflammatory, antivirus, prevention of colon cancer and mutations, immunomodulation and adsorption of heavy metals. With great development and utilization values, wheat bran has long attracted wide attention from Chinese and foreign scholars. The paper summarizes the latest advance in domestic and foreign studies on effective components in wheat bran and their pharmacological effect, and gives a brief introduction of the limiting factors in the comprehensive development and utilization of wheat bran, in order to provide new preference for the development and utilization of abundant wheat bran resources in China.
Animals ; Dietary Fiber ; analysis ; pharmacology ; Humans

Three butylphthalide derivatives were isolated from the Rhizome of Ligusticum chuanxiong using a series of isolation and purification approaches including macroporous resin, ODS-A column, Sephadex LH-20 and preparative HPLC. These structures were elucidated based on extensive spectroscopic data (UV, IR, HR-ESI-MS and NMR) and identified as (3Z,3aE)-(6R,7R,2'S)-6-hydroxy-7-(2-carboxyl-2-hydroxyethylthio)-3-(2-hydroxybutylidene)-4,5,6,7-tetrahydro-phthalide (1), (3Z,3aZ)-3-butylidene-6,7-dihydroxy-4,5,6,7-tetrahydro-phthalide 7-O-α-D-glucopyranosyl-(1→2)-β-D-fructo-furanoside (2) and 3-(3-β-D-glucopyranosyloxy-butylidene)-7-hydroxy-phthalide (3).

This study is to investigate the protective effect of longistyline A against corticosterone-induced neurotoxicity in PC12 cells. While PC12 cells were exposed to 100 micromol x L(-1) corticosterone for 48 h, cell survival rate was reduced and lactate dehydrogenase (LDH) release increased. In parallel, corticosterone caused significant elevations of DNA fragmentation, [Ca2+]i and caspase-3 activity. However, when the PC12 cells were incubated with longistyline A (4.0, 8.0 and 16.0 micromol x L(-1)) in the presence of 100 micromol x L(-1) corticosterone for 48 h, the effects were evidently alleviated, but dose-dependent manner was not obvious. In summary, longistyline A could generate a neuroprotective effect against corticosterone-induced neurotoxicity in PC12 cells possibly by decreasing [Ca2+]i and caspase-3 activity.
Animals ; Cajanus ; chemistry ; Calcium ; metabolism ; Caspase 3 ; metabolism ; Cell Survival ; drug effects ; Corticosterone ; toxicity ; DNA Fragmentation ; drug effects ; L-Lactate Dehydrogenase ; metabolism ; Molecular Structure ; Neuroprotective Agents ; isolation & purification ; pharmacology ; PC12 Cells ; Phenols ; isolation & purification ; pharmacology ; Plant Leaves ; chemistry ; Plants, Medicinal ; chemistry ; Rats

ObjectiveTo evaluate the efficacy of different dones of urapidil in preventing pituitrin-induced cardiovascular responses in patients undergoing laparoscopic myomectomy.MethodsSixty ASA Ⅰ or Ⅱ patients,aged 27-41 yr,weighing 55-65 kg,scheduled for elective laparoscopic myomectomy under general anesthesia,were randonly divided into 4 groups (n =15 each):control group (group C) and urapidil 0.3,0.5 and 0.8 mg/kg groups (groups U1-3).Urapidil 0.3,0.5 and 0.8 mg/kg were injected intravenously in U1-3 groups respectively,while normal saline 5 ml was given in group C.The mixture of pituitrin 6 U and normal saline 20 ml was injected into the site of hysteromyoma 5 min later.The operation was then started.BIS value was maintained at 45-55.The occurrence of cardiovascular responses was recorded.ResultsThe incidences of cardiovascular responses were 100％,67％,40％ and 20％ in groups C and U1-3 respectively.The incidence of cardiovascular responses was significantly lower in groups U1-3 than in group C,and in groups U2.3 than in group U1 ( P ＜ 0.01 ).There was no significant difference in the incidence of cordiovascular responses between U2 and U3 groups (P ＞ 0.05).ConclusionUrapidil can prevent pituitrin-induced cardiovascular responses in patients undergoing laparoscopic myomectomy and the optimal dose is 0.5 mg/kg.

Objective To approach the clinical presentation,treatment and diagnosis of primary seminal vesicle carcinoma.Methods The records of 4 patients who diagnosed seminal vesicle carcinoma were retrospectively reviewed,including the symptoms signs and examination results as well as operation program,postoperative therapy.Considered to the literature reports.Bilateral seminal vesicles,bladder, prostate and rectum were totally removed in one case.Seminal vosiculectomy and partial cystoprostotectomy were performed in 2 cases,and the another one,bilateral lower ureterectomy and ileum substitute bladder was be done.Results Followed up for 3 months to 5 years,and no recurrence had been observed so far, one died of colon cancer after 2 years.Conclusions Early symptoms of primary seminal vesicle carcinoma are unobvious,so that early diagnosis of seminal vesicle carcinoma is difficult and the misdiagnosis is so usually.Thus,accurate recognition is important for early diagnosis.Radical surgery appears to offer the best chance and different approaches can be selected according to tumor stage and invasive condition of the circumambient organ.Comprehensive treatment like hormonal therapy,along with the 5-fluorouracil,paclitaxel,and oxaliplatin chemotherapy regimen appears to be effective against adenocarcinoma.

ObjectiveTo compare the predictive value of anatomic scoring system, physiological scoring system, and the combination of two systems in death prediction of patients with severe trauma in intensive care unit (ICU). Methods A retrospective analysis of patients with severe trauma admitted to department of critical care medicine of Daping Hospital, the Third Military Medical University, and Zunyi Medical University from January 2011 to December 2014 was conducted. The patients meeting the following criteria were enrolled: over 16 years old, admitted to hospital shorter than 24 hours after trauma, length of ICU stay≥48 hours, and injury severity score (ISS)≥16. Patients were divided into two groups: survivors and non-survivors. The data of anatomic scoring system, including ISS and new injury severity score (NISS), and physiological scoring system, including acute physiology and chronic health evaluationⅡ(APACHEⅡ) score were collected. The predictive power for death of the scoring system alone or combination in patients with severe trauma was evaluated.Results A total of 614 patients with severe trauma were enrolled, and there were 153 deaths with a mortality rate of 24.9%. ISS, NISS, APACHEⅡ, ISS+ APACHEⅡ, NISS+ APACHEⅡ of non-survivors were significantly higher than those of survivors (ISS: 29.15±7.75 vs. 24.31±6.50, NISS: 41.96±12.01 vs. 29.64±8.19, APACHEⅡ: 23.71±6.58 vs. 17.02±5.49, ISS+ APACHEⅡ: 52.86±10.00 vs. 41.33±8.70, NISS+ APACHEⅡ: 65.67±13.46 vs. 46.66±10.43, allP< 0.01). The area under receiver operating characteristic curve (AUC) of ISS, NISS, APACHEⅡ, ISS+ APACHEⅡ, NISS+ APACHEⅡ was 0.687, 0.792, 0.782, 0.809, and 0.860, respectively. Both of ISS+ APACHEⅡ and NISS+ APACHEⅡ had higher AUC than that of ISS, NISS or APACHEⅡ alone; and the AUC of NISS+ APACHEⅡ was significantly larger than that of ISS+ APACHEⅡ(allP< 0.05). NISS+ APACHEⅡ showed the largest AUC in death prediction of severe trauma patients. The cut-off value, sensitivity, specificity, positive predict value (+PV), negative predict value (-PV), positive likelihood ratio (+LR), negative likelihood ratio (-LR), and Youden index of NISS+ APACHEⅡ, which had the greatest AUC, were 56, 75.2%, 82.0%, 58.1%, 90.9%, 4.17, 0.30, and 0.572, respectively.Conclusion The combination of anatomic scoring system and physiological scoring system is better than single scoring system for death prediction in patients with severe trauma in ICU, and it may be considered to be a new method for early identification of death risk in patients with severe trauma.

Tumor angiogenesis provides adequate oxygen and nutrition for tumor development and supports tumor growth and metastasis. Stromal cell derived factor 1 (SDF-1) and its receptor C-X-C motif chemokine receptor 4 (CXCR4) in pancreatic cancer microenvironment are involved in tumor growth such as promoting tumor cell proliferation, migration, and angiogenesis. In this study, anti-CXCR4 nanobody (CXCR4 Nb) and anti-programmed cell death ligand 1 (PD-L1) &CXCR4 bispecific nanobody (PX4 BsNb) were expressed in Escherichia coli system and purified by nickel column affinity chromatography. We investigated the anti-angiogenesis activity and mechanism of CXCR4 Nb by in vivo and in vitro experiments. Ethical approval was obtained for collection of human peripheral blood mononuclear cell (hPBMC) samples from the Local Ethics Committee of Shanghai Jiao Tong University. All animal experiments were approved by the Animal Ethic Committee of Shanghai Jiao Tong University. The results showed that CXCR4 Nb at 0.1 μmol·L^-1 could effectively inhibit the proliferation and migration of human umbilical vein endothelial cells (HUVEC) promoted by pancreatic stellate cells in vitro. CXCR4 Nb and PX4 BsNb at 0.3 mg·kg^-1 obviously decreased tumor angiogenesis and inhibited the tumor growth in NOD/SCID mice, the inhibitory rates were 28.8% and 36.1%, respectively. CXCR4 Nb significantly inhibited tumor growth and angiogenesis with great safety, which provides support for application of CXCR4 Nb and anti-angiogenesis therapy of pancreatic cancer.

OBJECTIVETo investigate the effect of small interfering RNA (siRNA) targeting human vascular endothelial growth factor (hVEGF) on A549 cell growth in nude mice and angiogenesis on chorioallantoic membrane (CAM) assay.

METHODSThree pairs of hVEGF siRNA-plasmid and non-silencing-plasmid were constructed, and transfected into A549 cells through lipofectamine 2000, respectively. The most effective pair of hVEGF siRNA-plasmid was selected by ELISA and real-time RT-PCR. A549 cells transfected with selected hVEGF siRNA- plasmid, A549 cells transfected with non-silencing-plasmid and A549 cells without transfection were inoculated into nude mice, respectively. Chick embryos were randomly divided into four groups and CAM was treated by different solutions for 48 h: culture media DMEM as negative control group,un-transfected A549 cell culture supernatants as positive control group, hVEGF siRNA A549 cell culture supernatants as hVEGF siRNA group and nonsilencing siRNA A549 cell culture supernatants as non-silencing siRNA group. The CAMs were harvested on d12 for microscopic assays.

RESULTCompared with control group, hVEGF siRNA-plasmid induced 48% reduction in hVEGF secretion by A549 cells accompanied by 70% reduction in hVEGF mRNA. Compared with non-silencing siRNA group, the mean tumor volume of murine xenograft was reduced by 58% in hVEGF siRNA group; time for xenografts growing to 50 mm(3)was delayed by 5.4 d. hVEGF contents in xenograft were reduced by 54%; but mean doubling time of tumors and the growth rate of tumors were not significantly reduced. In CAM assays, hVEGF content was zero in negative group, and in hVEGF siRNA group that was 40%-44% of non-silencing siRNA group or positive group; vessels branch points of CAM in hVEGF siRNA group or non-silencing siRNA group or positive group were increased by 45%-55% compared with negative group; total vessel length of CAM in hVEGF siRNA group was increased by 53% compared with negative group, while in non-silencing siRNA group or positive group that was increased by 97% or 99%. Compared with negative control group, the proliferation of microvessels was increased when cell culture supernatant with hVEGF was added in hVEGF siRNA group, significant proliferated vessels were observed in non-silencing siRNA group or positive group.

CONCLUSIONA plasmid-mediated hVEGF siRNA has been constructed and verified, which can effectively downregulate the expression of hVEGF in human A549 cells, resulting in the inhibition of angiogenesis. hVEGF siRNA can delay initial growth of A549 tumor xenograft but not reduce the growth rate.

Adenocarcinoma ; pathology ; Animals ; Cell Line, Tumor ; Cell Proliferation ; Chick Embryo ; Chorioallantoic Membrane ; blood supply ; metabolism ; Female ; Humans ; Lung Neoplasms ; pathology ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Neoplasm Transplantation ; Neovascularization, Physiologic ; RNA Interference ; RNA, Messenger ; genetics ; RNA, Small Interfering ; genetics ; Vascular Endothelial Growth Factor A ; antagonists & inhibitors ; genetics

OBJECTTo investigate the therapeutic effect of microencapsulated porcine retinal pigmented epithelial cells (RPE-M) transplantation on rat model of Parkinson's disease (PD).

METHODSPrimary porcine RPE cells were harvested by enzyme digestion and expanded in culture medium. Determine the levels of dopamine (DA) and homovanillic acid (HVA) by high performance liquid chromatography electrochemical (HPLC) assay, and the levels of brain-derived neurotrophic factor (BDNF) and glial-derived neurotrophic factor (GDNF) were detected by ELISA. Alginate-polylysine-alginate (APA) microencapsulated cells were produced by using a high voltage electrostatic system. PD rat model was established by unilateral injection of 6-hydroxydopamine (6-OHDA) into the medial forebrain bundle (MFB). After that, the RPE-M was transplanted into the corpus striatum of PD rat, and then the rotation test scores were recorded and biochemical changes of the corpus striatum were tested.

RESULTSThe levels of DA, HVA, BDNF and GDNF secreted by RPE were stable in the RPE culture supernatant and were not changed by the microencapsulation. Eighty-three percent rats developed PD by unilateral lesion of 6-OHDA in the MFB. The RPE-M transplantation had therapeutic effect on 33% PD rats.

CONCLUSIONPorcine RPE cells grow actively in vitro and could secrete DA, HVA, BDNF, and GDNF constantly, which does not be affected by the passage culture and the APA miroencapsulation. RPE-M transplantation of may be a curative therapy for PD.

Adrenergic Agents ; toxicity ; Animals ; Brain-Derived Neurotrophic Factor ; metabolism ; Cell Transplantation ; methods ; Cells, Cultured ; Disease Models, Animal ; Dopamine ; metabolism ; Enzyme-Linked Immunosorbent Assay ; Epithelial Cells ; metabolism ; transplantation ; Glial Cell Line-Derived Neurotrophic Factor ; metabolism ; Male ; Oxidopamine ; toxicity ; Parkinson Disease ; etiology ; surgery ; Rats ; Rats, Sprague-Dawley ; Retina ; cytology ; Swine ; anatomy & histology ; Time Factors ; Transplantation, Heterologous ; methods ; Tyrosine 3-Monooxygenase ; metabolism

OBJECTIVETo construct recombinant lentiviral vectors for gene delivery of the glial cell line-derived neurotrophic factor (GDNF), and evaluate the neuroprotective effect of GDNF on lactacystin-damaged PC12 cells by transfecting it into bone marrow stromal cells (BMSCs).

METHODSpLenti6/V5-GDNF plasmid was set up by double restriction enzyme digestion and ligation, and then the plasmid was transformed into Top10 cells. Purified pLenti6/V5-GDNF plasmids from the positive clones and the packaging mixture were cotransfected to the 293FT packaging cell line by Lipofectamine2000 to produce lentivirus, then the concentrated virus was transduced to BMSCs. Overexpression of GDNF in BMSCs was tested by RT-PCR, ELISA and immunocytochemistry, and its neuroprotection for lactacystin-damaged PC12 cells was evaluated by MTT assay.

RESULTSVirus stock of GDNF was harvested with the titer of 5.6 x 100,000 TU/mL. After transduction, GDNF-BMSCs successfully secreted GDNF to supernatant with higher concentration (800 pg/mL) than BMSCs did (less than 100 pg/mL). The supernatant of GDNF-BMSCs could significantly alleviate the damage of PC12 cells induced by lactacystin (10 micromol/L).

CONCLUSIONOverexpression of lentivirus-mediated GDNF in the BMSCs cells can effectively protect PC12 cells from the injury by the proteasome inhibitor.

Acetylcysteine ; analogs & derivatives ; pharmacology ; Animals ; Bone Marrow Cells ; cytology ; metabolism ; Cells, Cultured ; Culture Media, Conditioned ; metabolism ; DNA, Recombinant ; Genetic Therapy ; methods ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; genetics ; metabolism ; Lentivirus ; genetics ; Neurons ; drug effects ; Neuroprotective Agents ; metabolism ; PC12 Cells ; drug effects ; Plasmids ; genetics ; Protease Inhibitors ; pharmacology ; RNA, Messenger ; analysis ; Rats ; Rats, Sprague-Dawley ; Stromal Cells ; Transduction, Genetic ; methods