OBJECTIVETo investigate the expression of cortical SCF/KIT system at different blood glucose level in mice.

METHODS27 male C57 mice were randomly divided into control group, diabetes group, and diabetes plus insulin group. The diabetic mice were induced by streptozotocin. Western-blot and double-immunofluorescence histochemistry were used to detect the expression of SCF and KIT.

RESULTSBoth methods indicate that the level of S-SCF and M-SCF were decreased significantly in the diabetes group, and this trend can be reversed effectively when the insulin was utilized.

CONCLUSIONThe decline of SCF might be one of underlying mechanisms of diabetic encephalopathy.

Animals ; Cerebral Cortex ; metabolism ; Diabetes Mellitus, Experimental ; drug therapy ; metabolism ; Down-Regulation ; physiology ; Insulin ; therapeutic use ; Male ; Mice ; Mice, Inbred C57BL ; Proto-Oncogene Proteins c-kit ; metabolism ; Stem Cell Factor ; metabolism

OBJECTIVETo investigate the effects and the mechanisms of L-Arginine (L-Arg), the critical substrate for nitric oxide (NO) production, on pulmonary inflammatory cytokine expression and Nuclear Factor-kappa B signal pathway in a model of lipopolysaccharide (LPS) induced acute lung injury (ALI).

METHODSModel of ALI was induced by injection (iv) with LPS 5 mg/kg in male SD rats. L-Arg (500 mg/kg ip) was administrated at 3 h or 6 h after LPS injection respectively for 3 h, and the rats were killed at 6 h or 9 h after saline (control) or LPS injection. The expression and the translocation of NF-kappa B P65 in lung tissue were detected with immunohistochemisty (IHC). The gene expression of intercellular adhesion molecule-1 (ICAM-1) was examined by RT-PCR. The concentrations of TNF-alpha and IL-6 in lung tissue were respectively evaluated by radioimmunoassay. The pathological changes of lung tissue were observed by light microscope.

RESULTSCompared with LPS group, treatment with L-Arg at 3 h after LPS significantly decreased the expression of NF-kappa B protein. The concentrations of TNF-alpha and IL-6 in lung tissue were significantly decreased and the lung damage was inproved respectively compared with that of the LPS (3 h + 3 h) group. The lung damage was alleviated in L-Arg (3 h + 3 h) group.

CONCLUSIONRelatively early administration of L-Arg might protect lung from LPS-induced injury by inhibiting NF-kappa B activation and subsequently inhibiting the NF-kappa B-mediated release of inflammatory factors.

Acute Lung Injury ; chemically induced ; physiopathology ; prevention & control ; Animals ; Arginine ; pharmacology ; therapeutic use ; Inflammation ; physiopathology ; Interleukin-6 ; metabolism ; Lipopolysaccharides ; Male ; NF-kappa B ; metabolism ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; drug effects ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo observe the role of NB127914, a CRF R1 receptor antagonist, in the regulation of neonatal sleep/wake cycle.

METHODSRat pups were surgically implanted with electrodes at postnatal day(PN) 13. At PN 14, 6 hours polysomnographic recording data were continuously collected before and after administration of various doses of NBI 27914, atropine and the same amount of saline.

RESULTSCompared with baseline, rapid eye movement (REM) sleep was significantly reduced and was replaced primarily by non-REM (NREM) sleep in all groups treated with NBI, but not with dimethyl sulfoxide/saline. Atropine suppressed REM sleep significantly and increased wakefulness simultaneously.

CONCLUSIONBlockage of corticotropin-releasing factor (CRF) R1 receptors deprives neonatal rat REM sleep.

Aniline Compounds ; pharmacology ; Animals ; Female ; Male ; Polysomnography ; Pyrimidines ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Corticotropin-Releasing Hormone ; antagonists & inhibitors ; Sleep, REM ; drug effects ; physiology ; Wakefulness ; drug effects ; physiology

OBJECTIVETo demonstrate the inhibitory effect of kappa-opioid receptor activation by U50488H on hypertrophy induced by NE in cultured neonatal rat cardiac myocytes and compare its effect with that of prazosin and propranolol.

METHODSThe cellular proliferation was determined with crystal violet staining. The protein content was assayed with Lowry's method. The cardiomyocytes volumes were measured by computer photograph analysis system. The protein synthesis was assayed with [3H]-lencine incorporation method.

RESULTS(1) NE significantly induced the increase of protein content, [3H]-leucine incorporation and cell size without a concomitant increase in cell number in low serum medium. OThese responses were partially suppressed by prazosin or propranolol alone and completely abolished by both in combination. U50488H significantly inhibited the NE-induced increase of protein content, [3H]-leucine incorporation and cell size. The inhibitory effects of U50488H on NE-induced cardiac hypertrophy were greater than either prazosin or propranolol, but comparable to combination of both.

CONCLUSIONNE, acting via both alpha1- and beta-adrenergic pathway, stimulates myocyte hypertrophy. Stimulating kappa-opioid receptor significantly inhibits NE-induced cardiac hypertrophy, which may be related with alpha1- and beta1-adrenergic pathway.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer ; pharmacology ; Adrenergic alpha-1 Receptor Antagonists ; pharmacology ; Adrenergic beta-Antagonists ; pharmacology ; Animals ; Animals, Newborn ; Cardiomegaly ; chemically induced ; pathology ; prevention & control ; Cell Enlargement ; drug effects ; Cells, Cultured ; Female ; Male ; Myocytes, Cardiac ; cytology ; Norepinephrine ; Prazosin ; pharmacology ; Propranolol ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Opioid, kappa ; agonists

OBJECTIVETo probe the changes of fast component of brainstem auditory evoked potentials (FC-BAEP), slow component of brainstem auditory evoked potentials (SC-BAEP) and the mitochondrial ultrastructures of the neurons in the brainstem in the rat pups with hyperbilirubinemia.

METHODS7 days old SD rat pups were randomly divided into control group (C, 17 rat pups) and two test groups (T1, 17 rat pups and T2, 17 rat pups). Bilirubin solutions (2 g/L) were injected into the abdominal cavity of the rat pups in the group T1 and T2 at the postnatal day 7 and 10. Six hours after the second injection, seven rat pups of each group were randomly selected to test serum bilirubin concentration via a micro-gauge. FC-BAEP and SC-BAEP were examined with an evoked potential recorder in the rest rat pups of each group at postnatal day 17 and 20. At the postnatal day 20, the endocardial perfusion was performed in these rat pups for the fixation of the brain, and then the brains were taken out. The cochlear nuclei were used for observation via electron microscope.

RESULTSSix hours after the injection of bilirubin solution at the postnatal day 10, the serum bilirubin concentrations of the rat pups in group T1 and T2 were increased significantly. Except for II-IV inter-peak latency(IPL), all the peak latency(PL) and IPL of FC-BAEP evoked via three sound stimulating rates (10/s, 40/s,80/s) at the postnatal day 17 prolonged significantly in the rat pups of group T1 and T2, and the PL in group T2 were much longer than that in group T1. Except for II-IV IPL of FC-BAEP evoked via sound stimulating rates of 10/s and 40/s, all the PL and IPL at the postnatal day 20 prolonged significantly in the rat pups of group T1 and T2. The PL of SC-BAEP evoked via sound stimulating rate of 10/s at the postnatal day 17 and 20 in the rat pups of group T1 and T2 prolonged significantly, and the PL at the postnatal day 17 in group T2 were much longer than that of group T1. The changes of mitochondria of the neurons in the cochlear nuclei at the postnatal day 20 in the rat pups of group T1 and T2 were characterized by swell, the slurred membranes, the broken crista and so on.

CONCLUSIONThere were the abnormal changes of FC-BAEP, SC-BAEP and the mitochondrial ultrastructures of the neurons in the brainstem in the rat pups with hyperbilirubinemia. The PL and IPL of FC-BAEP and SC-BAEP could be taken as the objective and sensitive indexes for early monitoring the bilirubin-induced hearing loss and brain injury.

Animals ; Animals, Newborn ; Brain Stem ; pathology ; Evoked Potentials, Auditory, Brain Stem ; physiology ; Hearing Loss ; etiology ; physiopathology ; Hyperbilirubinemia ; complications ; physiopathology ; Male ; Mitochondria ; ultrastructure ; Neurons ; ultrastructure ; Rats ; Rats, Sprague-Dawley

Event-Related Potentials, P300 ; physiology ; Humans ; Individuality ; Male ; Memory, Short-Term ; physiology ; Neuropsychological Tests ; standards ; Young Adult

OBJECTIVETo observe the therapeutic time window of L-serine against focal cerebral ischemia/reperfusion injury in rats, and related mechanisms.

METHODSSprague-Dawley rats were randomly divided into six groups (n=6), sham-operation group, vehicle group, 3, 6, 12 and 24 h treatment group of L-serine. Focal cerebral ischemia was induced with the method of middle cerebral artery occlusion (MCAO) in rats, and reperfusion was emerged by removing the thread 2 h later. The treatment of L-serine (200 mg/kg ip) was begun at 3, 6, 12 and 24 h after MCAO respectively, and subsequently repeated once 12 h. The vehicle group was intraperitoneally injected with isodose normal saline. The neurological behavior score and cerebral infarction volume was measured 48 h after reperfusion. In addition, the contents of malondialdehyde (MDA), activity of superoxide dismetase (SOD), the levels of inflammatory cytokines (TNF-alpha, IL-6) and ultrastructure of neuron in brain tissue were investigated.

RESULTSCompared with the vehicle group, treatments with L-serine both 3 and 6 h after MCAO decreased the neurology deficit score and infarct volume. Only neurology deficit score had been reduced 12 h after MCAO, while no neuropmrotective effects had been observed during 24 h. Furthermore, L-serine elevated the content of SOD, decreased the level of MDA, TNF-alpha and IL-6 in ischemic brain tissue, and alleviated the injury of the neuronal ultrastructure.

CONCLUSIONL-serine exerted a time-dependent neuroprotective effect on the brain after MCAO in rat. This effect might be possibly mediated through following mechanisms: lessening oxidative stress and reducing the release of inflammatory cytokines.

Animals ; Brain Ischemia ; drug therapy ; pathology ; physiopathology ; Interleukin-6 ; metabolism ; Male ; Neuroprotective Agents ; therapeutic use ; Oxidative Stress ; drug effects ; Rats ; Rats, Sprague-Dawley ; Reperfusion Injury ; prevention & control ; Serine ; therapeutic use ; Superoxide Dismutase ; metabolism ; Time Factors ; Tumor Necrosis Factor-alpha ; metabolism

Animals ; Coxsackievirus Infections ; metabolism ; pathology ; physiopathology ; Enterovirus B, Human ; Female ; Glutathione Peroxidase ; metabolism ; Male ; Mice ; Myocarditis ; virology ; Oxidative Stress ; drug effects ; Selenium ; pharmacology ; Superoxide Dismutase ; metabolism

OBJECTIVETo investigate the effect and mechanism of meloxicam on the inflammatory reaction induced by beta amyloid protein (AB) in Alzheimer's disease (AD) rats.

METHODSThe rat model was established by microinjection of Abeta(1-40) into hippocampus. The expression of NF-kappaB p65 and glial fibrillary acidic protein (GFAP) in hippocampus were detected by immunohistochemistry. The content of GFAP in cortex was tested by Western-blot. The content of TNF-alpha in cortex was tested by ELISA. The expression of IL-1beta mRNA was tested by RT-PCR.

RESULTSThe expression of NF-kappaB p65, GFAP and TNF-alpha as well as IL-1beta mRNA were decreased by meloxicam.

CONCLUSIONMeloxicam can reduce the proliferation of astrocyte by decreasing the expression of GFAP in AD model rat's hippocampus and cortex. And the depression of NF-kappaB p65 may significantly decrease the expression of TNF-alpha1 and IL-1beta to lessen the inflammatory reaction in cerebral tissue.

Alzheimer Disease ; chemically induced ; drug therapy ; pathology ; Amyloid beta-Peptides ; toxicity ; Animals ; Cerebral Cortex ; metabolism ; pathology ; Glial Fibrillary Acidic Protein ; metabolism ; Inflammation ; prevention & control ; Interleukin-1beta ; metabolism ; Male ; Peptide Fragments ; toxicity ; Rats ; Rats, Sprague-Dawley ; Thiazines ; pharmacology ; therapeutic use ; Thiazoles ; pharmacology ; therapeutic use ; Transcription Factor RelA ; metabolism ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVETo study isolation and culture from SD rat bone marrow mesenchymal stem cells (rBMMSCs) and differentiate into endothelial-like cells (ELCs) with VEGF and bFGF.

METHODSIn vitro rBMMSCs were cultured with the method of percoll (1.073 g/ml) density centrifugation and adherence to plastic dishes. Then they were seeded in LG-DMEM supplemented with 10% fetal bovine serum. The relative biologic characteristics of rBMMSCs including cell morphology, phenotype, growth curve, cell cycle and ultrastructure were studied by inverted microscope, immunocytochemistry, flow cytometry, MTT method, transmission electron microscopy(TEM). The induced cells were identified by immunocytochemistry with CD31, CD34, CD144(VE-cadherin), FITC-UEA-1 and had ability in Dil-ac-LDL uptake and were observed under inverted microscope.

RESULTSThe morphology of rBMMSCs was spindle and has whirlpool. Growth curve of P4 showed that there was difference of latency, activity and flat periods. TEM showed that there were two of rMSCs , the small of both were infantile cells. GO/G1 phase of cell cycle was 95.67% and was suggested that most of cells were not in period of proliferation. The part differentiated cells demonstrated the characters of endothelial-like cells under inverted microscope and showed the expression of CD31, CD144, CD34, and possed the functions of endothelial-like cells staining double-positive for Dil-Ac-LDL and FTIC-UEA-1.

CONCLUSION1.073 g/ml percoll density centrifugation and cultured adherence is an effective approach to obtain rBMMSCs. In vitro, the cells have potential to differentiate into endothelial-like cells

Animals ; Bone Marrow Cells ; cytology ; Cell Differentiation ; physiology ; Cell Separation ; methods ; Cells, Cultured ; Endothelial Cells ; cytology ; Female ; Fibroblast Growth Factor 2 ; pharmacology ; Male ; Mesenchymal Stromal Cells ; cytology ; Rats ; Vascular Endothelial Growth Factor A ; pharmacology