Objective To study the effect of prolactin(PRL) on the activation of T lymphocytes stmiulated by concanavalin A(ConA),and to explore the action of PRL in the activation of T lymphocytes. Methods After CD4 +T cell line JurkatE6-1 cells were respectively stmiulated by 5 mg/L ConA,25 ?g/L PRL and 500 ?g/L bromocriptine(Brc).The blank control group,the ConA group,the PRL and ConA group(PRL group),the Brc and ConA group(Brc group),the PRL and Brc group(PRL-Brc group) were set in the experiment.The total RNA was extracted by Trizol after 48 hours and was reversed transcription immediately.The expression of tumor necrosis factor receptor associated factor 6(TRAF6) mRNA of T lymphocytes was checked by PCR.The expressions of tumor necrosis factor(ligand) super family 4(TNFSF4) and Killer specific secretory protein of 37 000(KSP37) mRNA of T lymphocytes were detected by real-time polymerase chain reaction. Results The PRL group and the Brc group could inhibit the expressions of TRAF6,TNFSF4,and KSP37 mRNA of the activated T lymphocyte compared with the blank control group and the ConA group(P a0.05).The PRL-Brc group could inhibit significantly the expressions of TRAF6,TNFSF4,and KSP37 mRNA of the activated T lymphocyte compared with the ConA group(P a

OBJECTIVETo observe the influences of FVP1 on both curative and negative effects of CTX.

METHODThe present study included two parts of experiments. In the part 1, 0.2 mL of 1 x 10(7) mL(-1) of S180 cells were inoculated in the subcutaneous layer of the right armpit of mice. All the mice were randomly divided into 3 groups: control group, in which mice were given with normal saline in 10 consecutive days, CTX group, in which mice were injected with 30 mg of CTX in the first and third days and saline in the other 8 days during the 10 consecutive days of treatment, and FVP1 and CTX group, in which the mice were injected with 30 mg x kg(-1) of CTX in the first and third days and FVP1 at 10 mg x kg(-1) in all 10 consecutive days of treatment. After above 10-day treatment , all the mice were killed and the tumor body was taken out and weighed to calculate the inhibiting rates on tumor. In the part 2 of experiments all the mice were divided into 3 groups: Normal control group, in which mice were not treated with any drugs, CTX-induced model group of inhibiting immune system, in which mice were injected with CTX at dose of 10 mg x kg(-1) in first two days and saline in the following 7 days; and small-, meddle-and large-dosage of FVP1 groups, in which mice were injected with CTX at the same dose as above in first two days and FVP1 intraperitoneally at 5, 10 and 20 mg x kg(-1) respectively in the following 7 days. CTX group was regarded as the control model. After the treatment, the peripheral white cells, thymus index, spleen index, the phagocytic power of macrophage of abdominal cavity, lymphocyte trastation rate and the activity of NK cell were detected.

RESULT(DFVP1 plus small dose of CTX obviously enhanced the inhibiting rate of CTX on tumor in the mice inoculated with S180 cells. (2) FVP1 at the different dose obviously antagozized CTX-induced leucopenia, atrophy, reduction of the phagocytic power of macrophage in abdominal cavity and restored the function of lymphocyte translation and the activity of NK cells.

CONCLUSIONFPV1 could enhance the curative effect of CTX in depressing tumor and attenuate the negative effect of CTX in inhibiting the function of immune system.

Agaricales ; chemistry ; Animals ; Antineoplastic Agents, Alkylating ; adverse effects ; pharmacology ; Cell Line, Tumor ; Cyclophosphamide ; adverse effects ; pharmacology ; Dose-Response Relationship, Drug ; Drug Synergism ; Killer Cells, Natural ; drug effects ; Leukopenia ; chemically induced ; Lymphocyte Activation ; drug effects ; Macrophages, Peritoneal ; physiology ; Mice ; Neoplasm Transplantation ; Phagocytosis ; drug effects ; Polysaccharides ; isolation & purification ; pharmacology ; Random Allocation ; Sarcoma 180 ; pathology

To study the preventive effect of Grifola frondosa on nonalcoholic steatohepatitis (NASH). The rat model of NASH was established by feeding high-fat diets for 12 weeks and intervened with 0.5 g · kg(-1) · d(-1) and 1.0 g · kg(-1) · d(-1) of C. frondosa powder suspensions. The degrees of hepatocyte fatty degeneration and inflammation were observed under the optical microscope with routine HE staining. The NAFLD activity scores (NAS) were calculated. Serum ALT, AST and hepatic TG and CHOL were tested by the biochemical method. The hepatic MDA was examined by thiobarbituric acid method. The hepatic SOD was tested by the xanthine oxidase test. The hepatic GSH-PX activity was determined by the dithio-nitrobenzoic acid method. Hepatic TNF-α and IL-6 were detected by the enzyme-linked immunosorbent assay (ELISA). The NASH model group induced by high-fat diets showed higher hepatic NAS, ser- um ALT, AST, CHOL and hepatic TG, CHOL, MDA, TNF-α, IL-6 (P < 0.01 or P < 0.05) and lower serum TG and hepatic SOD, GSH-PX (P < 0.01, P < 0.05) than the normal control group. After being intervened with different doses of G. frondosa, the NASH group revealed significantly lower hepatic NAS, serum ALT and hepatic TG, CHOL, MDA, TNF-α and IL-6 (P < 0.05) and higher hepatic SOD, GSH-PX (P < 0.05) than the model group. G. frondosa may prevent the further development of NASH by improving the disorder of lipid metabolism in rats with NASH induced by high-fat diets, relieving the level of oxidative stress and reducing the generation of inflammatory cytokines.
Animals ; Drugs, Chinese Herbal ; administration & dosage ; Grifola ; chemistry ; Humans ; Interleukin-6 ; metabolism ; Liver ; drug effects ; metabolism ; Male ; Non-alcoholic Fatty Liver Disease ; drug therapy ; metabolism ; Oxidative Stress ; drug effects ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo observe the effect of pure total flavonoids from Citrus (PTFC) on the hepatic fatty degeneration, inflammation, oxidative stress and SIRT1/PGC-1alpha expressions in mice with non-alcohol steatohepatitis (NASH), and discuss the action mechanism of PTFC on NASH.

METHODMice were given high-fat diet for 16 weeks to induce the NASH model. Since the seventh week after the model establishment, the mice were intervened with 100, 50 and 25 mg x kg(-1) x d(-1) PTFC for 10 weeks. The pathologic changes in hepatic tissues were observed with HE staining. The contents of TG, CHOL in hepatic tissue, as well as the levels of AST, ALT in serum were detected by using the biochemical process. The expression of SIRT1, PGC-1alpha and MnSOD mRNA in hepatic tissues were detected with Real-time PCR assay. SIRT1, PGC-1alpha protein and 8-OHdG expressions were determined with the immunohistochemical method. The SOD level in hepatic tissues was tested by the xanthine oxidase method. The MDA content in hepatic tissues was examined by the thiobarbituric acid method.

RESULTThe contents of TG, CHOL, NAFLD activity scores and ALT level in serum in hepatic tissues of mice in the model induced by fat-rich diet were obviously higher than that of the normal group (P < 0.010. The SIRT1, PGC-1alpha, MnSOD mRNA and protein expression in hepatic tissues were significantly lower than that of the normal group (P < 0.01). The expression of 8-OHdG and the content of MDA in hepatic tissues were obviously higher than that of the normal group (P < 0.01). After the intervention with different doses of PTFC, the NAFLD activity scores, the content of TG and the level of AST in serum were notably lower than that of the normal group (P < 0.01, P < 0.05); whereas the SIRT1, PGC-1alpha, MnSOD mRNA and protein expression were obviously higher than that of the normal group (P < 0.01, P < 0.05), with the significant decrease in the expression of 8-OHdG and the content of MDA (P < 0.01).

CONCLUSIONOxidative stress/lipid peroxidation enhancement in in NASH mice induced by high-fat diet may be related to the changes in SIRT1/PGC-1alpha signal transduction pathway. PTFC could enhance the anti-oxidant capacity in liver, relieve the damage of reactive oxygen during the fatty acid metabolic process, and prevent NASH from the occurrence and development by regulating the SIRT1/PGC-1alpha signal pathway.

Animals ; Citrus ; chemistry ; Fatty Liver ; drug therapy ; genetics ; metabolism ; Flavonoids ; chemistry ; pharmacology ; Inflammation ; drug therapy ; genetics ; metabolism ; Liver ; drug effects ; metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Non-alcoholic Fatty Liver Disease ; Oxidative Stress ; drug effects ; genetics ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Sirtuin 1 ; genetics ; metabolism ; Transcription Factors ; genetics ; metabolism

The identity of higher-order neurons and circuits playing an associative role to control renal function is notwell understood.We identified specific neural populations of rostral elements of brain regions that project multisynaptically to the kidneys in 3~ days after injecting a retrograde tracer pseudorabies virus (PRV)-614 into kidney of 13 adult male C57BL/6J strain mice.PRV-614 infected neurons were detected in a number of mesencephalic (e.g.central amygdala nucleus),telencephalic regions and motor cortex.These divisions included the preoptic area (POA),dorsomedial hypothalamus (DMH),lateral hypothalamus,arcuate nucleus (Arc),suprachiasmatic nucleus (SCN),periventricular hypothalamus (PeH),and rostral and caudal subdivision of the paraventricular nucleus of the hypothalamus (PVN).PRV-614/Tyrosine hydroxylase (TH) double-labeled cells were found within DMH,Arc,SCN,PeH,PVN,the anterodorsal and medial POA.A subset of neurons in PVN that participated in regulating sympathetic outflow to kidney was catecholaminergic or serotonergic.PRV-614 infected neurons within the PVN also contained arginine vasopressin or oxytocin.These data demonstrate the rostral elements of brain innervate the kidney by the neuroanatomical circuitry.

Objective To investigate the effect of lemon peel extracts(LPE) on the activity of lactate dehydrogenase and sucrase of Streptococcus mutans (Sm). Methods After serial dilution with trypticase soy broth (TSB) medium containing 2% glucose, LPE was used as the experimental group, and TSB without LPE as the control group. Sm was added to each group,which was then cultured for 6,18,24 and 48 hours in the anaerobic tank. The activity of lactate dehydrogenase (LDH) was measured with the method of oxidation of reduction coenzyme I and the pH value of the culture solution was also detected. The activity of the sucrose was determined with the method of coloration of 3,5-dinitrosalicylic acid. Results The activity of LDH, sucraae and the changes of solution pH were decreased with the increase of the concentration of LPE (P ＜ 0. 01 ). The activity of LDH were declined from (0. 8025 ± 0. 0913 ) × 103 U/L to (0. 2099 ±0. 0283) × 103 U/L; the activity of sucrase were declined from ( -0. 0107 ±0. 0003) × 103 U/L to ( -0.0078 ±0.0002) × 103 U/L; the△pH were declined from(2.8067 ±0.0404) to (2.5033 ±0. 0416) (24 h results). The differences were significant between experimental groups and the control group (P ＜ 0. 01 ), and there were also significant differences among experimental groups with different LPE concentration( P ＜0. 01 ). The inhibitory effect of acid generation and lactate dehydrogenas' activity of Sm were positively correlated ( P ＜ 0. 01 ). Conclusions LPE can inhibit the activity of lactate dehydrogenase,sucrase and the acid production capacity of the Sm in a dose dependent manner. The inhibitory effects in logarithmic phase is stronger than that in other phases of growth cycle.

OBJECTIVETo evaluate the feasibility and safety of nickel-titanium compression anastomosis ring (CAR27) in colorectal anastomosis after low anterior rectal resection in animal models.

METHODSEnd-to-end colorectal anastomosis was performed using CAR27 in 6 experimental pigs after resection of the middle and lower third of the rectum. The animals were observed postoperatively for up to 56 days. Five pigs were sacrificed at day 14 and the other at day 56. Distance from anal verge to anastomosis and anastomotic circumference were measured. Histopathologic examination was performed.

RESULTSThe median distance from anal verge was 5.3(4-6) cm. No anastomotic leak or other complications were observed. All the pigs recovered and gained weight. In 5 animals sacrificed at day 14, the mean circumference of the anastomosis was 6.8(6.5-7.0) cm, and histopathological examination showed mild inflammatory reaction and fibrosis. In the one sacrificed at day 56, the circumference expanded to 9.3 cm, and no inflammation and fibrosis were observed. Minor adhesion was noticed in only one pig, while smooth and intact serosa in the anastomosis was seen in the rest of the animals.

CONCLUSIONCAR27 is a promising device for mid and low colorectal anastomosis.

Anastomosis, Surgical ; instrumentation ; Animals ; Female ; Male ; Models, Animal ; Nickel ; Rectal Neoplasms ; surgery ; Rectum ; surgery ; Swine ; Swine, Miniature ; Titanium

BACKGROUNDThrombin is a multifunctional serine protease that plays a crucial role in hemostasis following tissue injury. In addition to its procoagulation effect, thrombin is also a potent mesenchymal cell mitogen, therefore it plays important roles in the local proliferation of mesenchymal cells in the tissue repair process. Reactive oxygen species (ROS) can induce some human cells to proliferate at lower rates while at higher concentrations they promote cells to undergo apoptosis or necrosis. Accumulative evidence suggests that thrombin can induce some cells to produce ROS. Based on these observations, we provide a hypothesis that thrombin can stimulate human lung fibroblasts to produce ROS, which play an important role in human lung fibroblast proliferation.

METHODSROS were detected in fibroblasts at 30 minutes and 60 minutes following thrombin (20 U/ml) exposure using flow cytometry. The ratio of reduced glutathione/oxidized glutathione (GSH/GSSG) was assayed in lung fibroblasts using a commercial kit following treatment with thrombin at different concentrations. NADPH oxidase and the extracellular regulated kinase1/2 (ERK1/2) signaling pathway were detected by Western blotting after thrombin stimulation to lung fibroblasts.

RESULTSThrombin, at 20 U/ml, stimulated human lung fibroblasts (HLF) to generate ROS in a time dependent manner. The ratio of GSH/GSSG in fibroblasts treated with thrombin showed a significant decrease. NADPH oxidase was activated and the ERK1/2 signal pathway was involved in the proliferation process of fibroblasts treated with thrombin.

CONCLUSIONThe activation of NADPH oxidase by thrombin leads to the production of ROS, which promotes fibroblasts proliferation via activation of the ERK1/2 signaling pathway.

Cell Proliferation ; drug effects ; Cells, Cultured ; Extracellular Signal-Regulated MAP Kinases ; analysis ; physiology ; Fibroblasts ; drug effects ; physiology ; Flow Cytometry ; Glutathione ; metabolism ; Humans ; Lung ; cytology ; NADPH Oxidases ; analysis ; physiology ; Reactive Oxygen Species ; metabolism ; Signal Transduction ; physiology ; Thrombin ; pharmacology

Cardiac Catheterization ; Heart Septal Defects, Ventricular ; therapy ; Humans ; Prosthesis Implantation ; instrumentation ; Septal Occluder Device

AIMTo determine whether the cardioprotection of ischemic postconditioning and heptanol in ischemic heart against ischemia/reperfusion (I/R) is mediated by gap junction.

METHODSThe effect of ischemic postconditioning, heptanol at different doses (0.03, 0.06, 0.30, and 0.60 mg/kg) and AAP10 (10 mg/kg) on the intact rat heart during 30 min ischemia and 2 h of reperfusion was observed. Ischemic postconditioning was achieved by 3 cycles of 10 s reperfusion/10 s regional ischemia starting at the beginning of the reperfusion. The infarct size and the arrhythmia scores were measured. The effect of ischemic postconditioning, heptanol at different doses (0.05, 0.10, 0.50 and 1.00 mmol/L) and AAP10 (1 x 10(-7)mol/L) on the isolated heart during 30 min ischemia and 2 h of reperfusion was observed. Ischemic postconditioning was achieved by 6 cycles of 10 s reperfusion/10 s global ischemia starting at the beginning of the reperfusion. The arrhythmia scores and conduction velocity of ventricle muscle were measured.

RESULTSIn the intact rat heart model, ischemic postconditioning and heptanol reduced infarct size and arrhythmia scores. In the Langendorff perfused rat heart model, ischemic postconditioning and heptanol reduced arrhythmia scores and conduction velocity of ventricle muscle. Administration of AAP10, an opener of gap junction attenuated the cardioprotection of ischemic postconditioning and heptanol.

CONCLUSIONThe cardioprotection of ischemic postconditioning and heptanol may be related to the attenuation of gap junction communication on myocardiac ischemia/reperfusion injury.

Animals ; Gap Junctions ; physiology ; Heptanol ; pharmacology ; Ischemic Postconditioning ; methods ; Male ; Myocardial Ischemia ; physiopathology ; Myocardial Reperfusion Injury ; physiopathology ; prevention & control ; Rats ; Rats, Sprague-Dawley