Objective To investigate the hepatoprotective effect of silybin-phosphatidylcholine complex(SPC) in sepsis rats.Me-(thods) Fifty Wistar immature rats were randomly divided into 3 groups:normal control(10 cases),septic group(30 cases) and interfe-(rence) group(10 cases).In septic group and interference group,rats were treated by cecal ligation and puncture(CLP).Meanwhile,the interference group was given SPC before 2 hours of CLP and after 2 hours of CLP.Blood of rats was taken from all groups to determine the levels of serum tumor necrosis factor-?(TNF-?),interleukin-1(IL-1),alanine aminotransferase(ALT) and aspartate aminotransferase(AST) at varying intervals.Results The levels of serum TNF-?,IL-1,ALT and AST after CLP were significantly elevated in septic group compared with the normal control group(P

Objective To observe the protective effect of silybin-phosphatidylcholine compound(SPC) on acute liver damage induced by alpha-naphthylisothiocyanate(ANIT) in mice.Methods Forty mice were randomly divided into 4 groups:normal group,model group,SPCⅠgroup,SPCⅡgroup.Intragastric administration of 0.5% carboxymethylcelluloes-Na(CMC-Na) suspension were given to the normal and model group,and 2 quantities of SPC suspension(150 and 300 mg/kg) were respectively given to SPCⅠ and SPC Ⅱ groups for 1 week.At 12 h after last administration of SPC,all of groups besides normal were given ANIT(dissolved in peanut oil,(60 mg/kg)) by lavage and the normal group just only were given peanute oil by the same volume and same way.After 16 h of ANIT administration,the levels of serum alanine transferase(ALT),aspartate aminotransferase(AST),serum total bilirubin(TB),malondialdehyde(MDA) and superoxide dismutase(SOD) were detected by biochemical method.Results Serum levels of ALT,AST,TB and MDA markedly increased after ANIT was administered via intragastric tube,and the level of serum SOD also decrease.SPC could obviously inhibit the alteration of the activities of serum ALT,AST,TB,MDA and SOD(P

As a renewable clean energy,biodiesel has been the subject of much research in recent years owing to its excellent environmental performance.The bio-enzymatic method possesses unparalleled advantages over conventional chemical catalysis,and it would be the direction in biodiesel industrialization process.The progress and application of three biocatalytic approaches for biodiesel production including immobilized lipase,free lipase and whole-cell catalysis were summerized.Finally,the challenges of biodiesel industrialization in China are analyzed,and some effective measures are put forward.

Objective To explore the effect of L-carnosine on neuronal cell apoptosis in young rats with experimental febrile seizures(FS).Methods Forty 15-day SD rats were randomly divided into intervention group(n=30)and FS group(n=10).Warm water was used to induce 10 times FS.The intervention group was divided into E,G and H group,10 rats in each group.Intraperitoneal injection of L-carnosine(250 mg/kg)was separately given to the rats in E group,G group and H group respectively after 30,60 and 120 min of seizure.FS group were induced FS,but they were not given intervention.The rats were sacrificed at 12 hours after the last seizure.Neuronal cell apoptosis was determined by terminal eoxynucleotidyl transferase-mediated dUTP nick end labeling(TUNEL)in situ cell death kit.TUNEL positive cells were stained and counted as apoptosis in hippocampus and cortex.Ultrastructural changes of apoptosis neurons were observed under the electron microscope.Results The neuronal cells apoptosis count was 25.37?1.95 in FS group,12.36?1.13 in E group,17.85?2.04 in G group,and 22.69?2.69 in H group.Neuronal apoptosis of FS group was apparently higher than that of interventional groups(F=10.75 P0.05).Under the electron microscope,neuronal damage on hippocampal CA1 area and dentate gyrus of FS group and H group was obviously higher than that of E group.Conclusions Early injection of L-carnosine would not only relieve neuronal apoptosis of repeated FS,but also play a role in the protection of neuronal cells.

0.05).Conclusions Early injection of L-carnosine would not only improve cerebral oxidative phosphorylation,relieve neuronal injury of repeated FS,but play a role in the protection of neuronal cells.

OBJECTIVETo explore attenuation and mechanism of endoplasmic reticulum stress (ERS)-mediated hepatocyte apoptosis in rats with alcohol-induced liver injury by Qinggan Huoxue Recipe (QGHXR) and its disassembled formulas (Qinggan Recipe and Huoxue Recipe respectively).

METHODSA rat model of chronic alcoholic liver injury was successfully established using a compound reagent of alcohol, corn oil, and pyrazol. The modeled rats were randomly divided into the model group, the QGHXR group, the Qinggan Recipe (QGR) group, and the Huoxue Recipe group (HXR). The CCl4 control group and the normal control group were also set up. There were ten rats in each group. All rats of modeled groups were gastrogavaged with alcohol compound reagent every morning. Rats in the QGHXR group (at the daily dose of 9. 5 g/kg, QGR group (at the daily dose of 3.0 g/kg), and HXR group (at the daily dose of 6.5 g/kg) were administered with corresponding medicines by gastrogavage every afternoon. Equal volume of normal saline was given to rats of the model group by gastrogavage. CCl4 was intraperitoneally injected at the dose of 0.3 mL/kg to rats in the CCl4 control group, once per week. Normal saline was given to rats in the normal control group by gastrogavage. The treatment was lasted for two weeks. Pathological changes of the liver were observed by histopathology. Serum total homocysteine (tHCY) level was detected by ELISA. The hepatocyte apoptosis rate was detected using flow cytometry. The gene and protein expressions of eukaryotic translation initiation factor 2 alpha (elF-2alpha), phosphorylation elF-2alpha (pelF-2alpha), glucose-regulated protein 78 (GRP78), and Caspase-3 in the liver were examined using Real-time PCR and Westen blot respectively.

RESULTSCompared with the normal control group, typical pathological changes of chronic alcoholic liver injury such as steatosis, inflammation, and even fibrosis occurred in model rats. The hepatocyte apoptosis obviously increased, with the apoptosis rate reaching the five-fold of that in normal rats. Besides, early apoptosis dominated. The serum tHCY level significantly increased. The expressions of p-elF-2alpha, GRP78, and Caspase-3 protein obviously increased (P < 0.01). Expressions of GRP78 and Caspase-3 mRNA significantly increased (P < 0.05, P < 0.01). Compared with the model group, the degrees of the liver injury and the hepatocyte apoptosis in the QGHXR group, the QGR group, and the HXR group were significantly alleviated. The serum tHCY level was significantly lowered. The protein expressions of p-elF-2a, GRP78, and Caspase-3 obviously decreased (P < 0.01). mRNA expressions of GRP78 and Caspase-3 obviously decreased in the QGHXR group (P < 0.05, P < 0.01). Only GRP78 mRNA expression obviously decreased in the QGR group (P < 0.05).

CONCLUSIONQGHXR and its disassembled formulas could attenuate ERS-mediated hepatocyte apoptosis in alcohol-induced liver injury rats by lowering the serum tHCY level and expressions of ERS apoptosis correlated factors.

Animals ; Apoptosis ; drug effects ; Caspase 3 ; metabolism ; Drugs, Chinese Herbal ; administration & dosage ; pharmacology ; therapeutic use ; Endoplasmic Reticulum Stress ; drug effects ; Eukaryotic Initiation Factor-2 ; metabolism ; Heat-Shock Proteins ; metabolism ; Hepatocytes ; drug effects ; pathology ; Homocysteine ; blood ; Liver Diseases, Alcoholic ; blood ; drug therapy ; pathology ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo study the role of inhibitor of differentiation 1 (ID1) in ATRA-induced acute promyelocytic leukemia (APL) cells differentiation.

METHODSThe expression of ID1 was detected by cDNA microarray, cycloheximide inhibition test, real-time RT-PCR and western blot.

RESULTSThe expression of ID1 gene was up-regulated in ATRA-induced NB4 cells and APL cells from two patients and was independent on other proteins synthesis. ID1 expression level reached the peak at 2 h in NB4 cells induced by ATRA, its relative expression level was (359.4 +/- 48.7)-fold greater than control. ID1 expression level reached the peak at 2 h in bone marrow cells from APL patents treated with ATRA, and its level detected 3 times in one of the patient was (311.1 +/- 48.7) fold of control. The expression of ID1 protein was not up-regulated in ATRA resistant NB4-R2 cells after ATRA treatment.

CONCLUSIONID1 may be involved in ATRA-induced granulocytic differentiation as an ATRA-targeted gene.

Antineoplastic Agents ; therapeutic use ; Cell Differentiation ; Humans ; Inhibitor of Differentiation Protein 1 ; genetics ; metabolism ; Leukemia, Promyelocytic, Acute ; drug therapy ; metabolism ; pathology ; Oligonucleotide Array Sequence Analysis ; Tretinoin ; therapeutic use

AIMThe characteristics of ryanodine receptor in rat cardiac sarcoplasmic reticulum (SR) and nuclear envelope (NE) were studied.

METHODSVelocity and isopyknic gradient centrifugation was employed to fractionate rat SR and NE. Ryanodine receptor was assayed with [3H] ryanodine saturate binding to the preparations.

RESULTSThe maximal binding (Bmax) and dissociating constant (Kd) of ryanodine receptor in rat cardiac NE were, 1.7% and 60% of those in SR respectively. Phosphorylation in vitro by PKA and PKC increased Bmax of the receptors in SR by 372% and 121%, and augmented those in NE by 221% and 306%, without any effects on Kd.

CONCLUSIONRyanodine receptors were present in rat myocardial NE, with lower density and higher affinity than those located in SR, which can be activated by PKA and PKC.

Animals ; Calcium ; metabolism ; Kinetics ; Myocardium ; metabolism ; Nuclear Envelope ; metabolism ; physiology ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Ryanodine ; metabolism ; Ryanodine Receptor Calcium Release Channel ; metabolism ; Sarcoplasmic Reticulum ; metabolism ; physiology

BACKGROUNDGlanzmann thrombasthenia (GT) is an autosomal recessive bleeding disorder characterized by the tendency to hemorrhage and the inability of platelets to aggregate in response to agonists. GT is caused by a defect of the platelet glycoprotein IIb/IIIa complex. The objective of this study was to describe the clinical features and the genetic cause of GT in a 6-year-old girl from south China.

METHODSA three-generation family was studied. The proband patient aged 6 years and her parents undertook examinations of platelet counts, blood film, bleeding time, platelet aggregation, and flow cytometry. All coding exons of the ITGA2B and ITGB3 genes were amplified by polymerase chain reaction (PCR), and direct sequencing was performed for mutational screening on the patient and normal controls consisted of 52 healthy blood donors. Reverse transcription PCR was conducted to test for exon skipping.

RESULTSThe proposita patient showed dispersing platelets, prolonged bleeding time, and severely reduced platelet aggregation in response to the physiological agonists adenosine diphosphate (ADP), epinephrine, collagen, and ristocetin. Flow cytometric measurements showed that the contents of alphaIIb and beta3 were significantly decreased. Sequencing results demonstrated two different types of heterozygous mutations existed in the alphaIIb gene (c.2930delG and IVS15-1delG). The compound mutations were also confirmed in the patient's mother and father separately.

CONCLUSIONSThe alphaIIbbeta3 deficiency of the proband was caused by two compound ITGA2B mutations, which were first reported in Chinese GT patients. The IVS15-1delG was first confirmed to cause an exon skipping.

Asian Continental Ancestry Group ; Child ; Female ; Flow Cytometry ; Heterozygote ; Humans ; Integrin alpha2 ; genetics ; Integrin beta3 ; genetics ; Mutation ; Pedigree ; Reverse Transcriptase Polymerase Chain Reaction ; Thrombasthenia ; genetics ; metabolism ; pathology

The purpose of this study was to investigate the effects of chloroquine diphosphate on the proliferation and apoptosis of human leukemic K562 cells, and to elucidate its possible mechanism of activity. The inhibitory effect of chloroquine diphosphate with different concentrations on K562 cell proliferation was detected by MTT method. Apoptosis was measured by flow cytometry (FCM); morphological analysis of apoptosis was performed after staining with propidium iodide (PI) under fluorescence microscope; cell apoptosis was assessed by the DNA ladder shown agarose gel electrophoresis. After treatment with chloroquine diphosphate, K562 cells were stained by Rhodamine 123 to detect changes in mitochondrial transmembrane potential (DeltaPsim) by FCM. The results showed that the cell viability decreased in dose-dependent manner, following chloroquine diphosphate treatment at different concentrations (1.5625, 3.125, 6.25, 12.5, 25, 50 and 100 micromol/L) for 24, 48 and 72 hours. By FCM analysis, the significant increases of sub-G(1) were observed. DNA ladder was detected and apoptotic nuclei were observed. DeltaPsim decreased in K562 cells after chloroquine diphosphate treatment. It is concluded that the chloroquine diphosphate can inhibit the proliferation of K562 cells and induce cell apoptosis, which may relate to down-regulation of mitochondrial transmembrane potential (DeltaPsim).
Antineoplastic Agents ; pharmacology ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Chloroquine ; analogs & derivatives ; pharmacology ; Dose-Response Relationship, Drug ; Down-Regulation ; drug effects ; Humans ; K562 Cells ; Membrane Potentials ; drug effects ; Mitochondria ; drug effects