In the paper, by taking acupuncture and migraine as the key words to retrieve CNKI and PubMed database, the literature analysis was done on the mechanism study on experimental migraine treated with acupuncture in rat model. The results showed that acupuncture mechanism study focused on the regulation and control of the relevant neurotransmitters/neuromodulators of migraine, such as calcitonin gene-related peptide (CGRP), serotonin (5-HT), nitric oxide (NO), etc. Moreover, in the paper, the review had been done on the neurotransmitters/neuromodulators involved in the study.
Acupuncture Points ; Acupuncture Therapy ; Animals ; Disease Models, Animal ; Humans ; Migraine Disorders ; genetics ; metabolism ; therapy ; Nitroglycerin ; metabolism ; Rats ; Serotonin ; metabolism

Coronary Disease ; etiology ; psychology ; Humans

Objective:To investigate the important role of the activation of complement system on the experimental hepatic necrosis.Methods:The complement activation of classic pathway was evaluated by detecting sexum CH50.The local hepatic deposition of C3 in rat hepatic necxosis was detected by immunohistochemical technique.Results:Compared with the controlled,serum CH50 decreased on different degree in all the administrated groups alone with prolonged observing time-page.Submassive hepatic necrosis was observed in Ga1N/LPS treated rats in H-E sections,and SP.Stainning showed the local hepatic deposition of C3 existed limited to the kupffer cells,the membrane,hepatocyte and the necrotic hepatocyte zone.GaIN caused gentle liver tissue injury,namly monocyie infiltration,hepatocyte balloon degeneration and focus necrosis,but none of deposition of C3 was observed.LPS caused the same changes as that by Ga1N,but the local hepatic deposition of C3 was limited to the endothelial cells and kupffer cells.Conclusion:The activation of complement in serum,especially the local hepatic activation of complement,play an important role in Ga1N/LPS-induced acute hepatic necrosis of rat.Extra-LPS may cause the activation of complement system the in classic activation of C3.Pathway of rat,but the hepatic injury may probably be related to the local hepatic deposion.Ga1N induced hepatic injury may has no direct relationship to the complement activation in serum.

3 ?g/well.All BALB/c mice immunized with pJME by im.and gene gun injection,and JE inactivated vaccines by ip.injection survived for 21 days.BALB/c mice immunized with pJE by im.injection and gene gun injection partially survived for 21 days.Titres of neutralization antibody produced with pJME were higher than pJE.Protective immunity and titre of neutralization antibody produced by im injection was the same as gene gun injection(im/gene gun injection: 1∶320/1∶320) at day 21.The antibody from BALB/c mice sera after twice pJME immunization only reacts with JEV-E protein. Conclusions Expression efficacy of proteins encoded by pJME and pJE in transfected cells is different.Expression level of related proteins was dependant on recombinant amount for transfection in a certain degree.Immunity effect induced with pJME was higher than pJE.The efficacy of DNA immunization produced by gene gun injection was higher than im.injection.Titres of neutralization antibody induced by DNA immunization were correlated to efficacy of protective immunity.Neutralization antibody from BALB/c mice sera produced by pJME immunization contained anti-E antibody against JEV-E protein.

OBJECTIVE:To establish a method for determining the concentration of vinorelbine bitartrate in human plasma, and study the pharmacokinetic process of vinorelbine in human plasma. METHODS:The samples were extracted with Solid-phase extraction(SPE). LC-MS/MS was performed on the column of Agilent Extend C18 with the mobile phase of 5 mmol/L ammonium ac-etate solution(pH10.5)-acetonitrile-methano1(18∶10∶72,V/V/V)at the flow rate of 0.4 ml/min,the ion source was ESI and MRM mode was used to scan positive ion detection. The ion reaction of quantitative analysis was m/z 779.50→m/z 122.10 (vinorelbine) and m/z 811.60→m/z 224.50 (internal standard, vinblastine). 3p97 was used to calculate the pharmacokinetic parameters. RE-SULTS:The determination was not interfered by endogenous impurities,and there was no matrix effect;the lowest limit of quantita-tive analysis was 2.0 ng/ml with the linear range of 2.0-4 000.0 ng/ml(r=0.997 8);the linear range of vinorelbine in plasma was. The intra-day and inter-day precisions and accuracy results were all in line with the acceptable limit across all concentrations. t1/2γ of 30 mg/m2,40 mg/m2 Vinorelbine Emulsion for Injection groups and 30 mg/m2 Vinorelbine for Injection group were(37.958 ± 34.256)、(47.835±54.231)、(76.873±40.537)h respectively,cmax were(1 426.250±397.562)、(1 700.125±624.669)、(2 187.500± 828.040)ng/ml respectively,AUC0-48 h were(75 839±19 551)、(82 088±14 207)、(95 318±18 208)mg·h/L respectively. CONCLU-SIONS:The method is rapid,sensitive and specific,and suitable for the determination of vinorelbine and pharmacokinetic study. Metabolic processes of vinorelbine can be described as first order process of three-compartment model in cancer patients.

Objective To investigate the changes of inositol 1,4,5-triphosphate receptor typeⅠ(IP3RⅠ)expression in the myocardial tissue of rats with endotoxic shock and probe the possible mechanisms of myocardial depression.Methods Thirty-three male Wistar rats were divided into four groups:control group (n=6) were injected normal saline(4ml/kg),and the other 3 groups (n=9) were injected endotoxin via femoral vein with a different dose of 10mg/kg,5mg/kg,and the artificial sacrificed group(10mg/kg,the rats were sacrificed when the mean arterial pressure was first rapidly decreased,then gradually increased to the normal level).IP3RⅠexpression in the myocardial tissue of rats was detected by immunohistochemistry,Western blot and colloidal gold immunoelectron microscopy technique.Results IP3RⅠexpressions were increased significantly in each group of rats with endotoxic shock than in the control group (P<0.01),and most obviously enhanced in the the artificial sacrificed group.The expression of IP3RⅠwas related to the level of mean arterial pressure.Ectopic expression of IP3RⅠwas observed around the cell membrane of the cardiac myocytes.Conclusion (1)The expression of IP3RⅠenhances in the myocardial tissue of rats with endotoxic shock,and exists ectopic expression.(2) The expression of IP3RⅠwas related to the level of mean arterial pressure.(3) IP3RⅠ may be related to the cardiac contractility and involved in the regulation of mean arterial pressure.

The inflammatory reaction after acute cerebral infarction can aggravate the cerebral ischemic reperfusion injury.Activation of peroxisome proliferator-activated receptors-γ(PPAR-γ) has neuroprotective effects by which induces anti-inflammatory actions in cerebral ischaemia,thus as a potential novel pharmacological target for ischemic stroke was regarded.Acupuncture can improve cerebral ischemia injury by inhibiting synthesis of inflammatory cytokines,downregulating expressions of inflammatory mediators and adhesion molecule,suppressing the functions of inflammatory cells.Therefore,it will be a promising orientation to sift the effective acupuncture for that can stimulate the activation of PPAR-γ,and the research of mechanism of acupuncture on anti-inflammatory reaction after cerebral ischemic by activating PPAR-γ dependent pathways.

Objective To explore the effects of TNF-α on the expression of IP3 R1 mRNA and protein in human mesangial cells (HMCs) and elucidate the role of protein kinase C (PKC) in this signal pathway.Methods Quantitative real-time polymerase chain reaction and immunoblot assay were used to examine the effects of TNF-α on IP3R1 mRNA and protein expression.Depletion PKC,the selective inhibitor of PKCα Safingol and inhibitor of PKCδ Rottlerin,overexpression of dominant negative mutant of PKC to examine the mechanism of signal transduction of TNF-α-regulated IP3 R1 in HMCs.PKCα activation was assayed by Western blot.Results TNF-α increased IP3R1 mRNA and protein expression in HMCs,effects that were blocked by prolonged incubted chronic PMA,Safingol and also by domain negative PKCα construct.TNF-α promoted PKCα activation with maximal PKCα phosphorylation that occurred 8 h post-stimulation.Conclusion TNF-α increased the expression of IP3 R1 and this was mediated through the PKCα activation signaling pathways in HMCs.

Objective To explore the expression change of intestinal epithelial tight junction (IJ)protein claudin-1 in mice with fulminant hepatic failure (FHF).Methods FHF was induced with a method that combined intraperitoneal injection of lipopolysaccharide (LPS,10 mg/kg) and D-galactosamine (GalN,800 mg/kg).Control saline (2 ml/kg,ip),LPS (10 mg/kg,ip) and GaIN (800 mg/kg,ip) were also detected.The effect of administration of anti-tumor necrosis factor alpha (TNF-α) IgG antibody (anti-TNF-α IgG,100 μg/per) on the level of TNF-α was assessed before administration of D-galactosamine/lipopolysaccharide.At the 2nd h,6th h,9th h,12th h,24th h after injection in FHF group,the 9th h after injection in control groups and 9th h after injection in anti-TNF-α IgG group,the mice were killed for the collection of large intestine specimens.Claudin-1 was analyzed with immunohistochemistry,Western blotting,and real-time quantitative PCR.Results Tight junction protein claudin-1 was localized along the apical region of the lateral plasma membrane representing the region of tight junctions in surface and crypt epithelial cells.Weakly distributed density of claudin-1 in intestinal mucosa was found in mice with FHF from the 9th h after injection.Compared to saline group,Western blotting analysis demonstrated markedly reduced claudin-1 expression in mice with FHF at the 6th h and 9th h after injection (6th h:0.8600±0.0208 vs 1.0,P ＜0.05; 9th h:0.6633 ±0.0328 vs 1.0,P ＜0.01).Furthermore,the expression of claudin-1 mRNA was markedly reduced at the 6th h,9th h,and 12th h after injection in mice with FHF (6th h:0.3067 ±0.1291 vs 1.0,P ＜0.05; 9th h:0.2233 ±0.1155 vs 1.0,P ＜0.01 ; 12th h:0.5275 ±0.1222 vs 1.0,P ＜0.05).Compared to saline group,no significant difference in claudin-1 expression was found with prophylactic treatment with anti-TNF-α-IgG antibody in mice with FHF at the 9th h after injection (protein:0.9533 ±0.0186 vs 1.0,P ＞0.05; mRNA:0.85 ±0.1437 vs 1.0,P ＞0.05).Conclusions The expression of tight junction protein claudin-1 was reduced at both protein and mRNA levels in intestinal epithelial cells that were induced by TNF-α in mice model of FHF.