Objective To study the protective effect of garlicin on radiation injury in mice. Methods Sixty mice were randomly divided into five groups:model control group, solvent control group and garlicin treatment groups[0.17, 0.33, 1.00 g/(kg?d)]. After treated by gavage for 20 consecutive days, the mice were exposed to 60Co-? irradiation for one time and the effect of the irradiation on the amounts of WBC in peripheral blood, the ratio of micronucleus cells in marrow, the content of DNA in marrow cells and the superoxide dismutase (SOD) activity were measured. Results Compared with the exposure group, garlicin increased the amounts of WBC, decreased the micronucleus frequency of marrow cells, increased the content of DNA in marrow cells and increased the SOD activity in mice. Conclusion Garlicin shows a protective effect on irradiation injury in mice.

rAdinbitor was cloned from Gloydius blomhoffi brevicaudus in the laboratory. Previous researches had proved that rAdinbitor could inhibit proliferation of C6 glioma cells as well as promote their apoptosis. The molecular mechanism of rAdinbitor’s effects on C6 cells need to be further studied. rAdinbitor was expressed in E. coli BL21/pET23b-adinbitor and purified with Ni Sepharose 6 Fast Flow. The purified protein was confirmed by Western blotting. C6 cells were induced with fibronectin (FN). The effects of rAdinbitor with different concentrations on the expression of FAK, MEK1/2 and Caspase-3 as well as on activity of FAK and ERK1/2 in FN-induced C6 cells were studied by immunoblotting and immunoprecipitation. Results showed that rAdinbitor with different concentrations could obviously reduce the expression of FAK and MEK1/2, increase the expression of Caspase-3, as well as decrease ERK1/2 phosphorylation; besides 10 mg/L rAdinbitor, other concentrations’ rAdinbitor could inhibit FAK phosphorylation obviously. All those effects were dose-dependent. Results indicate that the effects of rAdinbitor on decreasing expression and activity of FAK and inhibiting Ras-MAPK signaling pathway play an important role in suppressing the proliferation of C6. Furthermore, the increase in Caspase-3 expression implies that the increase in apoptosis of C6 cells might be due to the suppression of rAdinbitor on the activity of ILK and PI-3K/Akt pathway.

This paper discusses the current prevalence of hospital preparations backward quality standard test methods, quality standards for lack of a serious problem , and analyses the reasons from four aspects , proposed to strengthen the construction of a pharmaceutical ethics; examination and approval departments shall strictly agents registration review technical requirements;rectify and improve the quality of all preparation standards;Introduction and training of strengthen pharmacy personnel , and actively improve the quality standard revision work;hospital in-creasing hardware and software construction , support quality standards revision suggestions for the improvement of work, provide reference standard for quality improvement of hospital preparations .

OBJECTIVETo explore the neuroprotective effect and mechanism of picroside II on extracellular regulated protein kinases1/2 (ERK1/2) signal transduction pathway in cerebral ischemia injuryrats. METHODS The middle cerebral artery occlusion (MCAO) model was established by inserting a monofilament into middle cerebral artery. Totally 96 successfully modeled Wistar rats were divided into the modelgroup, the treatment (picroside II) group, the Lipopolysachcaride (LPS) group, and the U0126 group according to random digit table. Each group was further divided into 3 subgroups, i.e. 6, 12, and 24 h sub-groups. Picroside II (20 mg/kg) was peritoneally injected to rats in the treatment group 2 h after ischemia.LPS (20 mg/kg) and Picroside II (20 mg/kg) were peritoneally injected to rats in the LPS group 2 h after ischemia. U0126-EtOH (20 mg/kg)and Picroside II (20 mg/kg) were peritoneally injected to rats in the U0126group 2 h after ischemia. Equal volume of normal saline was peritoneally injected to rats in the control groupand the model group. The neurobehavioral function was evaluated by modified neurological severity score(mNSS) test. The structure of neurons was observed using hematoxylin-eosinstaining (HE) staining. Theapoptotic cells were detected using terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. The expression of phosphorylated extracellular signal-regulated protein kinase1,2 (pERK1,2) in cortex was detected using immunohistochemistry (IHC) and Western blot.

RESULTSAfter cerebral ischemia injury neurological impairment score increased, the damage of neuron in the cortical area was aggravated, apoptotic cells increased in the model group as time went by. The expression of pERK1/2 increased more significantly in the model group than in the control group (P <0.05). The damage of neuron in the cortical area was milder, while apoptotic cells decreased, the expression of pERK1f2 obviously decreased more in the treatment group and the U0126 group (P < 0.05). The early damage of neuron in the cortical area was more severe, apoptotic cells and the expression of pERK12 were comparatively higher in early stage of the LPS group, but the expression of pERK1/2 was somewhat decreased in late stage.

CONCLUSIONSActivating ERK12 pathway could mediate apoptosis and inflammatory reactions of neurons after cerebral ischemia injury. Picroside II could protect the nerve system possibly through reducing activation of ERKI2 pathway, inhibiting apoptosis of neurons and inflammation reaction.

Animals ; Apoptosis ; Brain Ischemia ; drug therapy ; Cinnamates ; pharmacology ; Infarction, Middle Cerebral Artery ; drug therapy ; Iridoid Glucosides ; pharmacology ; MAP Kinase Signaling System ; drug effects ; Neurons ; pathology ; Neuroprotective Agents ; pharmacology ; Random Allocation ; Rats ; Rats, Wistar

Objective:To observe the effect of acupuncture on blood oxygen concentration in the brain of rats with post-traumatic stress disorder (PTSD) based on functional near-infrared spectroscopy (fNIRS),thus to reveal the mechanisms of acupuncture in intervening the brain function of PTSD rats.Methods:Sixty Sprague-Dawley (SD) rats were randomly divided into a blank group,a model group,a grasping group,a paroxetine group and an acupuncture group,with 12 rats in each group.Except the blank group,rats in the other groups all received incarceration plus electric shock for 7 d to prepare the PTSD animal model.One hour before the stress model was established,rats in each group received the designated intervention:rats in the blank group and the model group did not receive any intervention;rats in the grasping group received grasping and fixation;rats in the paroxetine group received paroxetine hydrochloride solution by intragastric administration;and rats in the acupuncture group received acupuncture.Six-day treatment was a course,with 2 courses of treatment conducted for a total of 12 d.After the modeling,rats in each treatment group received intervention for 5 d,and the fNIRS system was used to collect and record the changes in the concentrations of oxygenated hemoglobin (HbO2),deoxygenated hemoglobin (d-Hb) and total hemoglobin (t-Hb) of the involved rat's brain regions,and also to assess the brain function.Results:Compared with the blank group,the concentration of HbO2 was significantly increased,the concentration of d-Hb was significantly decreased,and the concentration of t-Hb was significantly increased in the model group and the grasping group after the intervention,and the differences were statistically significant (all P＜0.01).Compared with the model group,the concentrations of HbO2,d-Hb and t-Hb in the grasping group did not change significantly (all P＞0.05).Compared with the grasping group,the concentration of HbO2 was significantly decreased,the concentration of d-Hb was significantly increased,and the concentration of t-Hb was significantly decreased in the paroxetine group and the acupuncture group,and the differences were statistically significant (all P＜0.05).There were no significant differences in the concentrations of HbO2,d-Hb and t-Hb between the paroxetine group and the acupuncture group (all P＞0.05).Conclusion:Acupuncture can regulate the blood oxygen concentration in the brain of PTSD model rats,which may be an important mechanism of acupuncture in intervening the brain function in PTSD rats.

Five compounds (tenuifoliside C, tenuifoliside D, telephiose A, telephiose C and polygalaxanthone III) from polygala tenuifolia wild were incubated together with CYP probe substrate in human liver microsomes to investigate the inhibitory effect towards CYP450 enzyme. Phenacetin (CYP1A2), coumarin (CYP2A6), paclitaxel (CYP2C8), diclofenac (CYP2C9), S-mepheriytoin (CYP2C19), dextromethorphan (CYP2D6), chlorzoxazone (CYP2E1), midazolam (CYP3A) were selected as the isoforfn specific substrate. And the formation of paracetamol, 7-hydroxycoumarin, 6alpha-hydroxy paclitaxel, 4'-hydroxydiclofenac, dextrorphan, 6-hydroxychlorzoxazone, 1'-hydroxymidazolam, 4'-hydroxymephenytoin were detected respectively to measure the effect towards CYP450 by high-pressure liquid chromatography (HPLC). The result shows that five compounds from polygala tenuifolia willd significantly inhibit chlorzoxazone 6-hydroxylation catalyzed by CYP2E1, while showed no effect towards CYP1A2, CYP2A6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP3A. And IC50 value was 38.73, 54.14, 61.77, 62.22, 50.56 micromol x L(-1), respectively.
Cytochrome P-450 Enzyme System ; metabolism ; Esters ; pharmacology ; Glycosides ; pharmacology ; Humans ; Microsomes, Liver ; drug effects ; enzymology ; Oligosaccharides ; pharmacology ; Polygala ; chemistry ; Xanthones ; pharmacology

Objective To study the relationship of clinical manifestation and pathological changes and prognosis in Henoch-Schonlein purpura nephritis(HSPN)in children.Methods Clinical and pathological characteristics of 42 children with HSPN were analysed.Among them,40 children were detected of angiotensin-convertion enzyme(ACE)gene and had been followed up.Results Among them,there were 9 cases of level Ⅰof pathological types,21 cases of level Ⅱ,12 cases of level Ⅲ,but no cases of level Ⅳ.Ⅰand Ⅱ level were found in those cases of clinical manifestation with solitary hematuria and albuminuria.Pathological grades were Ⅰ,Ⅱ and Ⅲ levels in the cases of hematuria and albuminuria.Pathological types of nephrotic syndrome(NS)were Ⅱ and Ⅲ level,which were of more gross hematuria than those of other grades.ACE gene DD had serious pathological damnification.Conclusions Change of pathology cannot only be anticipated by clinical manifestation of HSPN.But if pathological damnification gets more serious,the albuminuria gets more serious.Gross hematuria and albuminuria can serve as indicators of biopsy.NS of ACE DD type have serious pathological damnification.Children with HSPN has favourable prognosis in the future.

Objective Using Intelligence Scale of Mini Mental State Estimated (MMSE) as the gold standard to determine the relevance of International HIV-associated Dementia Scale (IHDS)in minority ethnic areas in Guangxi populations with different cultural values.Corresponding boundary value related to the authenticity and reliability on IHDS were also evaluated.Methods 200 patients with HIV infection were randomly selected from the minority ethnic groups in Guangxi.For each infected person,MMSE and IHDS blind scale were tested at the same period.Using the results from MMSE scale test as the gold standard,ROC curve and IHDS scale in Guangxi minority populations with different education levels which related to the diagnosis of dementia-HIV values were determined.The value of a specific sector under the IHDS sensitivity,specificity,and internal consistency coefficients was also evaluated.Results When considering the infected person did not differ on their educational level,the IHDS scale diagnostic cutoff appeared as 8.25,while 1HDS sensitivity as 0.925,specificity as 0.731 and Kappa as 0.477 (P＜0.001).When considering the extent of cultural differences did influence the prevalence of infection,the different education groups showed different IHDS diagnostic cutoff values.People with high school,secondary school or higher education levels,the IHDS diagnosis appeared to be 8.25,when sensitivity was 0.917,specificity was 0.895 and Kappa was 0.722 (P＜0.001).People with only primary education level,the IHDS appeared to be 7.25.When sensitivity was 0.875,specificity was 0.661 and Kappa was 0.372 (P＜0.001).Conclusion The IHDS diagnostic sector in Guangxi minority groups was lower than the internationally recommended level of diagnostic cutoff value (IHDS≤ 10 points).When using IHDS to perform the HIV related dementia screening program,in the minority areas of Guangxi,culture context,the degree and difference of HIV infection should be considered,especially in using IHDS diagnostic cutoff values.

OBJECTIVETo observe the effects of soluble epoxide hydrolase inhibitor t-AUCB on foam cell formation and cholesterol efflux in macrophage.

METHODSMouse macrophages RAW264.7 were cultured and stimulated with ox-LDL (80 µmol/L) in the absence (group A) or presence of t-AUCB (1, 10, 50, 100 µmol/L, group B) or t-AUCB (100 µmol/L) pretreated with PPARγ antagonist GW9662 (5 µmol/L, group C). The foam cell was identified by oil red O staining. The cholesterol efflux rates of (3)H-cholesterol in cells were measured by liquid scintillation counter. mRNA and protein expressions of ABCA1 were detected by real-time PCR or Western blot, respectively.

RESULTSOil red O staining showed that t-AUCB (100 µmol/L) significantly inhibited foam cell formation which could be significantly reversed by GW9662 (all P < 0.05). t-AUCB dose-dependently increased cholesterol efflux rates in mouse macrophage [(5.91 ± 0.18)% in group A, (7.03 ± 0.33)%, (8.05 ± 0.32)%, (9.04 ± 0.14)%, (10.06 ± 0.85)% in 1, 10, 50, 100 µmol/L t-AUCB groups, all P < 0.05 vs. group A], which could be reversed by pretreatment with GW9662 [(6.33 ± 0.15)% in 100 µmol/L t-AUCB + GW9662 group].t-AUCB also upregulated ABCA1 mRNA and protein expressions in a dose-dependent manner which could be significantly attenuated by pretreatment with GW9662.

CONCLUSIONt-AUCB could inhibit foam cell formation by improving cholesterol efflux through activating PPARγ-ABCA1 pathway in macrophage.

ATP Binding Cassette Transporter 1 ; ATP-Binding Cassette Transporters ; metabolism ; Animals ; Benzoates ; pharmacology ; Cell Differentiation ; drug effects ; Cell Line ; Cholesterol ; metabolism ; Enzyme Inhibitors ; pharmacology ; Epoxide Hydrolases ; antagonists & inhibitors ; Foam Cells ; drug effects ; Macrophages ; cytology ; drug effects ; metabolism ; Mice ; PPAR gamma ; metabolism ; Urea ; analogs & derivatives ; pharmacology

Aim To investigate the role of p38 mitogen-activated protein kinases(MAPKs) in genistein-induced osteoblastic differentiation of mouse bone marrow-derived mesenchymal stem cells(BMSCs).Methods Mouse BMSCs cultured in phenol red-free ?-MEM containing 10% V/V FBS,were added ?-glycerophosphate and ascorbic acid for inducing osteoblastic differentiation,and treated with 0.01~1 ?mol?L~(-1) genistein and/or SB203580 and PD98059.The temporal sequence of osteoblastic differentiation in BMSCs cultures was assayed by measuring alkaline phosphatase activity(ALP) and calcium deposition.The MAPK phosphorylation level was detected by Western-blot.Results Genistein(0.01~1 ?mol?L~(-1)) showed a dose-dependent effect on osteoblastic differentiation as evidenced by increased alkaline phosphatase(ALP) activity and calcium deposition in mouse BMSCs cultures.Genistein(1 ?mol?L~(-1))-induced osteoblastic differentiation of BMSCs was diminished by p38 MAPK inhibitor but not the p44/42 MAPK inhibitor.The effects of Genistein were associated with rapid and sustained activation of p38 MAPK in the BMSCs cultures,which was blocked by SB203580(1 ?mol?L~(-1)).In contrast,Genistein treatment resulted in inactivation of p42/44MAPK,which was further attenuated by PD98059(25 ?mol?L~(-1)).Conclusion p38 MAPK plays an important role in genistein-induced osteoblastic differentiation of mouse BMSCs cultures.