Animals ; Brain ; metabolism ; physiopathology ; Brain Ischemia ; genetics ; metabolism ; pathology ; Gene Expression ; Male ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley

BCG Vaccine ; adverse effects ; Child ; Child, Preschool ; Genetic Diseases, X-Linked ; complications ; Granulomatous Disease, Chronic ; complications ; genetics ; Humans ; Infant ; Infant, Newborn ; Lymphadenitis ; etiology ; Male ; Membrane Glycoproteins ; genetics ; NADPH Oxidase 2 ; NADPH Oxidases ; genetics

2 g/L can′t excluded SCID.

OBJECTIVETo study whether alisol B could inhibit complement 3a (C3a) induced renal tubular epithelial-mesenchymal transition (EMT).

METHODSThe in vitro cultured human renal tubular epithelial HK-2 cells were intervened with 5 ng/mL transforming growth factor-beta (TGF-beta), 0.1 micromol C3a, and 0.1 micromol C3a + 10 micromol alisol B, respectively. The mRNA and protein expressions of alpha-SMA, E-cadherin, and C3 were detected using RT-PCR, Western blot, and immunofluorescence, respectively.

RESULTSThe mRNA and protein expressions of C3 in HK-2 cells were up-regulated after intervention of C3a (P < 0.01), the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously enhanced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously decreased (P < 0.01). When compared with the group intervened by exogenous C3a, after intervention of alisol B, the mRNA and protein expressions of alpha-SMA in HK-2 cells were obviously reduced (P < 0.01), the mRNA and protein expressions of E-cadherin obviously increased (P < 0.05).

CONCLUSIONSExogenous C3a could induce renal tubular EMT. Alisol B was capable of suppressing C3a induced EMT.

Actins ; metabolism ; Cadherins ; metabolism ; Cell Differentiation ; drug effects ; Cell Line ; Cholestenones ; pharmacology ; Complement C3a ; metabolism ; Epithelial Cells ; drug effects ; metabolism ; Epithelial-Mesenchymal Transition ; drug effects ; Humans ; Kidney Tubules ; cytology ; metabolism

OBJECTIVETo study the protective effect of astragaloside IV on oxidative damages of Chang Liver cells induced by ethanol and H2O2.

METHODThe alcoholic and nonalcoholic oxidative damage models were established on Chang Liver cells with ethanol and H2O2, respectively. The cells viabilities were detected by MTT assay, transaminase activity and antioxidant ability were detected by micro plate and colorimetric method, reactive oxide species (ROS) was detected by DCFH-DA fluorescent probe and cell cycle was detected by flow cytometry. DNA ladder method was used to detect apoptosis.

RESULTBoth kinds of oxidative damage could decrease the viability and antioxidant enzyme activity of Chang Liver cells, and increase the transaminase activity and MDA content of extracellular fluid. The protective effects of astragaloside IV against those two kinds of oxidative damages were significant or extremely significant. Meanwhile, ethanol could decline the level of ROS significantly in the damaged cells, while H2O2 could increase it significantly. And the effect of astragaloside IV was to make ROS return to the normal level. Retardation of cell cycle progression of Chang Liver cells in G0/G1 induced by ethanol or H2O2 was relieved, and apoptosis was also inhibited.

CONCLUSIONAstragaloside IV had protective effect on oxidative damages of Chang Liver cells induced by ethanol and H2O2.

Antioxidants ; metabolism ; Apoptosis ; Cell Cycle ; drug effects ; Cell Line ; Cell Survival ; drug effects ; Ethanol ; pharmacology ; Humans ; Hydrogen Peroxide ; pharmacology ; Oxidative Stress ; drug effects ; Reactive Oxygen Species ; metabolism ; Saponins ; pharmacology ; Triterpenes ; pharmacology

Multi-target drugs attract increasing attentions for the therapy of complicated neurodegenerative diseases. In this study, a computer-assisted strategy was applied to search for multi-target compounds by the pharmacophore matching. This strategy has been successfully used to design dual-target inhibitor models against both the acetylcholinesterase (AChE) and poly (ADP-ribose) polymerase-1 (PARP-1). Based on two pharmacophore models matching and physicochemical properties filtering, one hit was identified which could inhibit AChE with IC50 value of (0.337 +/- 0.052) micromol x L(-1) and PARP-1 by 24.6% at 1 micromol x L(-1).
Acetylcholinesterase ; metabolism ; Cholinesterase Inhibitors ; pharmacology ; Computer-Aided Design ; Drug Discovery ; methods ; Poly(ADP-ribose) Polymerase Inhibitors

Dimethyl sulfide (DMS) has been historically recognized as a metabolite of the marine microorganism or a disgusting component for the smell of halitosis patients. In our recent study, DMS has been identified as a cytoprotectant that protects against oxidative-stress induced cell death and aging. We found that at near- physiological concentrations, DMS reduced reactive oxygen species (ROS) in cultured PC12 cells and alleviated oxidative stress. The radical-scavenging capacity of DMS at near-physiological concentration was equivalent to endogenous methionine(Met)-centered antioxidant defense. Methionine sulfoxidereductase A (MsrA), the key antioxidant enzyme in Met-centered defense, bound to DMS and promoted its antioxidant capacity via facilitating the reaction of DMS with ROS through a sulfonium intermediate at residues Cys72, Tyr103, Glu115, followed by the release of dimethyl sulfoxide (DMSO). MTT assay and trypan blue test indicated that supplement of DMS exhibited cytopro?tection against 6-hydroxydopamine and MPP + induced cell apoptosis. Furthermore, MsrA knockdown abolished the cytoprotective effect of DMS at near- physiological concentrations. The present study reveals new insight into the potential therapeutic value of DMS in Parkinson disease.

AIM: To analyze the genotype of the allele distribution of a polymorphic G-954C within the 5 upstream promoter region of the nitric oxide synthetase 2A gene (NOS2A) in samples of diabetic retinopathy in patients with cystoid macular edema in the mainland of China.METHODS: Eighty-nine patients with diabetic retinopathy and cystoid macular edema and 90 healthy controls were enrolled in this study. Nest polymerase chain reaction (PCR)was performed, and restriction endonudease digestion and gene fragments sequence were examined to detect the genotype of NOS24 G-954C.RESULTS: The genotypes of the sample population of 89 cases and 90 healthy controls were all detected as GG.CONCLUSION: The distribution of G-954C of NOS2A polymorphism are at a lower frequency in China, with little relevancy to the frequency of diabetic retinopathy combined with cystoid macular edema.

Objective To compare 99Tcm-MIBI MPI with delayed enhancement MRI (DE-MRI) in patients with idiopathic dilated cardiomyopathy (IDCM). Methods Forty patients with IDCM were included. They underwent both rest 99Tcm-MIBI myocardial perfusion imaging and DE-MRI within 7 days. 99Tcm-MIBI MPI was performed to identify diffuse or segmental abnormal perfusion patterns including reduced or defect perfusion segments. DE-MRI images were divided into 4 categories: no delayed enhancement, septal, subendocardial and transmural delayed enhancement, x2 test was used for data analysis. Results Diffuse and segmental perfusion abnormality on 99Tcm-MIBI MPI were found in 19 (47.5%) and 21 (52.5%)patients respectively, while DE-MRI enhancement was simultaneously found in 5 patients of the former (5/19, 26.3%) and 18 (18/21, 85.7%) of the latter (x2 =14.401, P＜0. 001). For those (n=18) with both segmental perfusion abnormality and DE-MRI enhancement, the number of segments of the 4 DE-MRI respectively. A significant difference was found in the DE-MRI enhancement categories between normal and defect perfusion segments (x2 = 29. 183, P ＜0.001 ) and between reduced and defect perfusion segments as well (x2 =25. 110, P＜0. 001). Conclusions Both diffuse and segmental perfusion abnormalities on 99Tcm-MIBI MPI can be found in patients with IDCM. DE-MRI enhancement is more frequently found in patients with segmental perfusion abnormality.

0.05); serum HBsAb levels of pregnant mice and neonatal mice in group with CpG-1826 (20 ?g)+hepatitis B vaccine significantly higher than those in group with CpG-1826 (10 ?g, 40 ?g)+ hepatitis B vaccine,hepatitis B vaccine and control respectively(P0.05).Conclusions Combination injection of CpG-1826 20 ?g and hepatitis B vaccine can markedly increase serum antibody levels of pregnant mice and neonatal mice, but don′t affect the survival quantity, the growth and development of neonatal mice.CpG-1826 is an ideal immune adjuvant for neonates with immature immune system during pregnancy.