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

Adolescent ; Adult ; Busulfan ; therapeutic use ; Female ; Hematopoietic Stem Cell Transplantation ; methods ; Humans ; Male ; Middle Aged ; Transplantation Conditioning ; methods ; Young Adult

Apgar Score ; Autopsy ; Fatal Outcome ; Heart Neoplasms ; diagnosis ; diagnostic imaging ; pathology ; Heart Ventricles ; diagnostic imaging ; Humans ; Infant, Newborn ; Male ; Myxoma ; complications ; diagnosis ; diagnostic imaging ; pathology ; Rare Diseases ; Ultrasonography

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

The origin and development of umbilical therapy in traditional Chinese medicine is explored from related literature in the history. As a result, the Shang period is regarded as initial period of umbilical therapy, while periods from Han Dynasty, Jin Dynasty and Southern-Northern Dynasties to Sui Dynasty and Tang Dynasty could be taken as stage of primary development. Time from Song Dynasty, Jin Dynasty and Yuan Dynasty to Ming and Qing Dynasties is believed as mature stage. Also the manipulation, application principle, indications and contraindications of umbilical therapy are explained. A brief overview of modern development of umbilical therapy is also described.
China ; History, 15th Century ; History, 16th Century ; History, 17th Century ; History, 18th Century ; History, 19th Century ; History, 20th Century ; History, Ancient ; History, Medieval ; Humans ; Medicine in Literature ; Medicine, Chinese Traditional ; history ; methods ; Umbilicus ; physiology

Animals ; Cardiovascular Diseases ; etiology ; metabolism ; Humans ; Inflammation ; metabolism ; Periodontitis ; complications ; metabolism ; microbiology ; Platelet Aggregation ; physiology ; Porphyromonas gingivalis ; pathogenicity ; RNA, Messenger ; metabolism ; Receptor, PAR-1 ; metabolism ; Receptor, PAR-2 ; genetics ; metabolism ; Receptors, Proteinase-Activated ; metabolism ; Receptors, Thrombin ; metabolism

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.

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.