Objective To investigate the effects of dexamethasone(DEX)on the secretion of interleukin (IL)-17 and interferon(IFN)-γ and the proportion of Th17,Tc17,Th1 ,Tc1 cells in peripheral blood mononuclear cells(PBMCs)of patients with systemic lupus erythematosus(SLE). Methods Thirty hospitalized SLE patients were recruited and twenty-two healthy volunteers were recruited as healthy controls. PBMCs were separated from SLE patients and healthy controls and then was cultured in vitro by medium or PMA/Ionomycin or PMA/Ionomycin +dexamethasone for six hours. Four- color immunofluorescent staining and flow cytometric assay were used to analyze the percentage of Th17,Tc17,Th1,Tc1 cells in PBMCs. Concentrations of IL-17 and IFN-γ in plasma and the supernatants of PBMCs which were cultured for 24 hours were measured by enzyme linked immunosorbent assay (ELISA). Results The plasma concentrations of IL-17 and IFN-γwere elevated in SLE patients as compared to the controls(P ＜ 0.05). No significant differences were observed between patients and controls for the spontaneous production of IL-17 and IFN-γ or percentage of T subsets expressed by PBMCs. After the stimulation of PMA,compared with the controls,the level of IL-17 was significantly elevated in the supematants of PBMCs and the percentages of Th17 and Tc1 in SLE patients increased significantly(P ＜ 0. 05). However,there showed no significant differences between SLE patients and the controls for the percentages of Th1 and Tc17 cells. DEX could significantly decrease the production of IL-17(P ＜ 0. 01)and the percentages of Th17,Tc1 cells by the active PBMCs(P ＜ 0. 05). Conclusions There is abnormal expression of T subset cells and their cytokines in vivo of SLE patients. DEX can interfere with immunological pathological process in the cytokine network imbalance of SLE patients and shows powerful inhibition of IL - 17. Our results may provide some laboratory evidence for the clinical application of corticosteroids.

Brain ; pathology ; Humans ; Infant, Newborn ; Lung ; pathology ; Male ; Seizures ; etiology ; pathology ; Tomography, X-Ray Computed ; Tuberous Sclerosis ; complications ; pathology

This study was aimed to discuss the distribution and protein expression level ofμ-opioid receptor (MOR) in hippocampus of premenstrual syndrome (PMS) liver-qi stagnation rat model, in order to initially reveal the action mechanism of PMS liver-qi stagnation and intervention effect ofShu-Yu (SY) capsule. Chronic restraint stress method was used to copy PMS liver-qi stagnation rat model.SY capsule ofTiao-Gan prescription was given as intervention. Immunofluorescence (IF) and western blot (WB) technique were used to detect MOR in hippocampal CA1 and CA3 brain area of rats from each group. The results showed that compared with the normal group, the hippocampus MOR distribution arrangement was messy with increased protein concentration in the model group (P< 0.01). After drug intervention, the MOR protein level returned to normal level. It was concluded that the pathogenesis of PMS liver-qi stagnation may be associated with high expression of MOR in hippocampus CA1 and CA3 region of rats. SY capsule can effectively correct and restore it to nearly normal level. It may be one of the central mechanisms in SY capsule treatment of PMS liver-qi stagnation.

Glucagon-like peptide 1(GLP-1) is an important member of incretin.Takingitoralymay stimulate the terminal ileum and colon L cel s to secrete GLP-1. After GLP-1 biding specific receptor GLP-1 receptor ( GLP-1R), it exerts the roles of promoting glucose-dependent insulin secretion, inhibiting glucagon secretion, and decreasing plasma glucagon level. The molecular mass of GLP-1 is relatively smal er and can directly cross the blood-brain barrier, and both central and peripheral nervous systems have the GLP-1R expression. GLP-1 significantly improves neurological deficits and reduces infarct volume. It may exert neuroprotective effect through the mechanisms of inhibiting the inflammatory response, oxidative stress, and cel apoptosis. This article review s the discovery of GLP-1, its biological characteristics and neuroprotective effect in cerebral ischemia.

Objectives To investigate the effects of matrine on the proliferation and apoptosis of SK-NEP-1 cells in vitro, and its possible mechanism. Methods Trials were divided into following groups:control group, 0.5, 1.0 and 1.5mg/ml of ma-trine intervention groups. The inhibition rate of SK-NEP-1 cells treated with different concentration of Matrine was detected by MTT colorimetric assay. Apoptosis rate was detected by flow cytometry (FCM). RT-PCR analysis was employed to measure the PDCD4 mRNA expression. Results Matrine (final concentrations=0.5, 1.0 and 1.5mg/ml) could induce apoptosis and inhibit the growth of SK-NEP-1 cells. Compared with the controls without matrine treatment (8.81±3.71)%, the inhibition rates of SK-NEP-1 cells were (20.79 ± 6.20)%, (31.25 ± 5.07)%, and (51.15 ± 12.70)%, respectively;the apoptotic rates of SK-NEP-1 cells treated with different concentration of matrine were (13.67±0.78)%,(17.43±1.65)%and (20.80±1.54)%, respectively. Significant difference in the inhibition and apoptotic rates of SK-NEP-1 cells between each drug group and control group was observed(P<0.05), and the inhibition and apoptotic rates of SK-NEP-1 cells increased gradually with increased matrine concentration, thus exhibiting a dose-dependent effect(P<0.05). To the expression of CXCR4 mRNA,the grey levels of SK-NEP-1 cells treated with matrine intervention group (final concentrations=0.5, 1.0 and 1.5 mg/ml) were (0.720 ± 0.058), (0.540 ± 0.095) and (0.307 ± 0.050), respectively. The mRNA expression of CXCR4 was seen in SK-NEP-1 cells. Compared with control group, the expres-sion of CXCR4 mRNA was decreased significantly in matrine intervention group (P<0.01).There were significant difference in CXCR4 mRNA level among the SK-NEP-1 cells treated with 0.5,1.0,1.5mg/mL of matrine (P<0.01). Conclusions Matrine could induce apoptosis and inhibit the growth of SK-NEP-1 cells in a dose-dependent way which may be associated with the down-regulated CXCR4 expression in SK-NEP-1 cells.

Burns, Inhalation ; complications ; Humans ; Male ; Middle Aged ; Nitric Acid ; adverse effects ; Pulmonary Edema ; chemically induced ; therapy

AIM: To investigate the anti-proliferative and apoptosis-inducing effect of honokiol on U937 cell line in vitro. METHODS: Proliferation of U937 cells and PBMCs were analyzed by MTT assay. Flow Cytometry and cell morphological observation were performed to find out whether honokiol could affect cell cycle and induce apoptosis of U937 as well as PBMCs in vitro. RT-PCR and Western blotting techniques were used to detect the changes in mRNA expression and protein production of bcl-2 and bax in U937 cells after treated with honokiol. RESULTS: Honokiol could significantly inhibit the proliferation of U937 cells at IC_ 50 concentration of 11.8 ?g/mL, but slightly inhibit the proliferation of PBMCs, at IC_ 50 concentration of 40.3 ?g/mL, respectively. Most honokiol-treated cells were arrested at G_0/G_1 phase. CONCLUSION: Honokiol could inhibit the proliferation and induce apoptosis of U937 cells, while has little effect on the proliferation and survival of PBMCs. Bax might be involved in the gene regulation related to honokiol-induced apoptosis.

OBJECTIVE:To establish a method for the determination of 1,1-ethanediol diacetate and acetic acid in flurbiprofen axetil. METHODS:Capillary gas chromatography was performed on the column of DB-FFAP capillary column by temperature pro-grammed,the inlet temperature was 150 ℃,flame ionization detector was chosen,detector temperature was 290 ℃,carrier gas was nitrogen at a flow rate of 1.0 ml/min,injection volume was 1.0 μl,and split ratio was 5∶1. RESULTS:1,1-ethanediol diacetate and acetic acid were well-separated;and the linear ranges was 0.78-19.55 g/ml(r=0.999 7)and 7.69-64.11 μg/ml(r=0.999 3),re-spectively;the limits of quantification were 0.78 μg/ml and 7.69 μg/ml,and limits of detection were 0.23 μg/ml and 2.56 μg/ml for 1,1-ethanediol diacetate and acetic acid respectively;RSDs of precision and reprocudibility tests were lower than 3%,and stability test was lower than 5%;recoveries were 97.6%-100.4%(RSD=0.94%,n=9)and 93.6%-100.4%(RSD=0.94%,n=9);and the test results for 3 batches of flurbiprofen axetil were met the specification. CONCLUSIONS:The method is simple,accurate and re-liable,and can be used for the determination of 1,1-ethanediol diacetate and acetic acid in flurbiprofen axetil.

Objective To provide a new putative target for immunotherapy on osteosarcoma and explore the effect of matrix metalloproteinase-9 (MMP-9) on the formation of soluble MICA protein in osteosarcoma cells. Methods MMP-9 antisense oligonucleotide was transfected to osteosarcoma cells with lipofectamine 2000. MMP-9 mRNA was assessed by RT-PCR. MMP-9 activity and soluble MICA (sMICA) in the culture supernatant was examined by zymography and quantified by ELISA, respectively. Results MMP-9 mRNA expression and gelatin enzymatic activity were inhibited in MMP-9 antisense oligonucleotide group. Comparing with the control group, lower concentration of sMICA was found in MMP-9 antisense oligonucleotide group (P = 0.011). Conclusion MMP-9 may have an effect on the formation of sMICA protein in osteosarcoma. MMP-9 could be regarded as a putative target for immunotherapy in osteosarcoma.