Promoting effects of Guavenoic acid (GA)on proliferation,insulin synthesis and secretion in INS-1 cells and their mechanism / 中国药理学通报

Aim To investigate the effects of Guaveno-ic acid (GA)on proliferation,insulin synthesis and secretion in INS-1 cells and their possible mechanism. Methods INS-1 βcells were cultured in vitro.Control group,medium group,model group,drug groups and positive group were set.INS-1 cells were treated with GA (0.3,1 ,3,1 0,30 nmol·L -1 )for 48 h.The cell proliferation was tested by MTT assay.Acid-alco-hol was used to extract the insulin in the cells and the amount of insulin synthesis of INS-1 cells was tested by RIA.5.6,1 6.7 mmol·L -1 glucose was used to chal-lenge INS-1 cells for 1 h to the insulin secretion model (BIS and GSIS)was tested,and the insulin secretion of INS-1 cells was tested via RIA.The mRNA expres-sion of insulin gene,PDX-1 and MafA was tested by q-PCR.Results Compared with medium group,GA could promote the proliferation of INS-1 cells signifi-cantly (P <0.01 )and promote the synthesis of insulin in INS-1 cells significantly (P <0.01 ).GA(0.3 ~30 nmol· L -1 )could promote the BIS,GSIS of INS-1 cells significantly (P <0.05 or P <0.01 ).GA (3,30 nmol·L -1 )could up-regulate the mRNA expression of insulin gene,PDX-1 ,MafA in INS-1 cells signifi-cantly (P <0.01 ).Conclusions GA could signifi-cantly improve the proliferation of INS-1 cells and pro-mote the insulin synthesis and secretion of INS-1 cells, which may be associated with up-regulation of insulin gene,PDX-1 ,MafA mRNA expression.

Effects of chloride channel blockers on H_2O_2 induced apoptosis in pancreas RIN-m beta cells / 中国药理学通报

Aim To investigate the effects of chloride channel blockers on the apoptosis of RIN-m? cells of pancreatic islet induced by H2O2.Methods The apoptotic model was made by H2O2 exposed for six hours with a concentration of 500 ?mol?L-1.The chloride channel blockers:DIDS,NPPB and NFA were administered to pretreat the samples respectively.The cell viability,morphological changes,and apoptosis rate were observed.Results Chloride channel blockers alone have no marked effects on the cell viability of RIN-m? cell.However,they elevated the cell viability of RIN-m?cell disposed of by H2O2.Compared to H2O2 group,the groups of DIDS +H2O2,NPPB+ H2O2 and NFA+H2O2 have significant difference in cell viability and apoptosis rate(P

SC58125 modulates TNF-?-induced HT-29 cells apoptosis through inhibiting I?B? degradation / 中国药理学通报

Aim To investigate whether SC58125 synergized with TNF-? to induce HT-29 cell apoptosis and study the possible molecular mechanism. Methods By using MTT, agarose gel electrophoresis and flow cytometry, we examined the effect of SC58125/TNF-? on cell proliferation and apoptosis in HT-29 cells. The activity of caspase-3 and the changes of I?B? and NF-?B were also measured after treatment with SC58125 by Electrophoretic mobility shift assay and Western blot. Results Both SC58125 and TNF-? exhibited cytotoxicity, the combination of the two agents significantly reduced HT-29 cell viability in a dose-dependent manner. TNF-?-treated cells showed oligonucleosomal cleavage of genomic DNA. SC58125 significantly enhanced the inhibition of cell proliferation and inducement of cell apoptosis of TNF-?,the apoptotic index was increased from 11.2%?1.1% to 53.9%?2.1%. SC58125/TNF-?-induced apoptosis of HT-29 cells was accompanied by the induction of caspases-3. I?B? levels were substantially decreased after treatment with TNF-? and the degradation of I?B? was almost completely inhibited when SC58125 was added in NF-?B was activated in HT-29 cells after treatment with TNF-?, whereas pretreatment of HT-29 cells with SC58125 for 2 h, TNF-?-induced NF-?B DNA binding was profoundly inhibited. Conclusion SC58125 synergizes with TNF-? to inhibit cell growth and induce apoptosis in HT-29 cells, which may be mediated by activating caspases and preventing degradation of I?B?.

Study on cobra venom factor / 中国病理生理杂志

Cobra venom factor (CVF), separated from the cobra venoms, is an acidic glucoproteins with anticomplementory activity. The combination of CVF with factor B in the blood produces a stable C3 and C5 converterase resulting in complement depletion by activating complement continually. There are many studies on it, such as inflammation, autoimmune disease, xenotransplantation, anti-tumor, etc. CVF is also an important tool drug for the study of complement role in the pathophysiological development of diseases.

Mechanisms of PGF_ (2?) on the glucose-induced insulin secretion in NIT-1? cells / 中国病理生理杂志

0.05). However, in the presence of 16.5 mmol/L glucose, PGF_ 2? increased significantly in insulin secretion (P

Changes of potassium channels in thoracic aorta of streptozotocin-induced diabetic mice in early stage / 中国病理生理杂志

AIM: To investigate the changes of potassium channels in thoracic aorta of streptozotocin-induced diabetic mouse in the early stage of diabetes mellitus. METHODS: The effects of 60 mmol/L KCl, phenylephrine (PE), sodium nitroprusside (SNP) were measured and concentration-response curves to SNP were determined in the presence and in the absence of the inhibitors of potassium channels on the thoracic aortic rings of diabetic and age-matched control mice in vitro. RESULTS: STZ-diabetic mice showed a significant increase in the maximum contractile response and sensitivity of thoracic aorta to 60 mmol/L KCl and PE. The endothelium-independent relaxation response to SNP was increased by diabetes and were decreased significantly by pretreatment of the vessels with 1 mmol/L tetraethylammonium (TEA), 1 mmol/L 4-aminopyridine (4-AP) and 10 ?mol/L glibenclamide in diabetes thoracic aorta. Only 4-AP decreased relaxation response to SNP in age-matched control mice. The -logIC 50 difference of TEA in thoracic aorta rings of diabetes was significantly higher than age-matched control mice.CONCLUSION: In early stage of diabetes mellitus, the opening or expression of K Ca channels is significantly enhanced.The opening of K ATP channels is also enhanced in this stage.

Inhibition of proliferation and apoptosis in HL60 cells induced by cobra venom serum / 中国药理学通报

AIM To explore the effects and mechanism of cobra venom serum on the proliferation in HL60 cells. METHODS Established the HL60 cells as a target to study the growth feature by the action of cobra venom serum.The agarose gel electrophoresis and flow cytometry analysis were used to demonstrate apoptosis. RESULTS Compared with the control group, the cells were inhibited significantly by the action of cobra venom serum.A characteristic DNA "ladder" was detected by using agarose gel electrophoresis. By flow cytometry analysis,it was proved that most apoptosis of HL60 cells occurred when cultured with cobra venom serum. CONCLUSION Cobra venom serum inhibited the HL60 cells in vitro , which was related to apoptosis. This may introduce a new way to the treatment of leukemia.

Effects of PGF2? on the glucose-stimulated insulin secretion in NIT-1 beta cells / 中国药理学通报

Aim To investigate the effects of PGF_(2?) upon glucose-stimulated insulin secretion and the calcium response in NIT-1 beta cells.Methods Using the radioimmunoassay(RIA),the amount of PGF_(2?) augmentation of glucose-stimulated insulin secretion was determined in different conditions and the confocal laser scanning methods by Fluo-3AM as a fluorescent probe were used to analyze the NIT-1 beta cell intracellular calcium response in correlated various terms.Results In the presence of 16.5 mmol?L~(-1) glucose,PGF_(2?)(0.1,1,5 ?mol?L~(-1)) dose-dependently augmented glucose-induced insulin secretion in NIT-1 beta cells,especially at 5 ?mol?L~(-1)(P0.05).Meanwhile,Exposure of the NIT-1 cells to 5 ?mol?L~(-1) PGF_(2?) induced a rapid increase of intracellular calcium(P

THE EFFECT OF CLONIDINE ON THE PGF_(2?) LEVELS IN THE BRAIN CORTEX OF MICE SUBJECTED TO CEREBRAL ISCHEMIA / 中国药理学通报

Prostaglandin F2? ( PGF2? ) in the brain cortex was measured in mice which were devided into 3 groups, ie sham operation group, cerebral ischemia group and reperfusion after cerebral ischemia group, treated with saline or clonidine ( 0 .15~1 .Omg/kg ) , respectively. The results showed that the PGF2? level in the ischemia group treated with saline was higher than sham operation group, but the PGF2? level in reperfusion group was the highest in all groups. Compared with saline, clonidine decreased the PGF2? levels either in the ischemia group or the reperfusion group significantly . This may be useful to attenuate the brain lesion caused by PGF2? .

Effects of ganoderma spores on apelin expression in rats with myocardial ischemia injury induced by isoproterenol / 中国病理生理杂志

AIM:To investigate the changes of apelin in blood and myocardium, and the protective mechanisms of ganoderma spores on myocardial ischemia injury induced by isoproterenol in rats. METHODS: The model of myocardial ischemia injury was induced by subcutaneous injection of high dose isoproterenol. Enzyme linked immunosorbent assay (ELISA) was used to measure the apelin contents in blood and myocardium. Semi-quantitative RT-PCR was used to measure the apelin mRNA level in myocardium. Electron microscope was used to observe the pathomorphological changes of myocardium. Ganoderma spores was administered i.g. for 7 weeks. RESULTS: Compared with the normal control group, the apelin contents in blood and myocardium and the apelin mRNA level in myocardium were significantly decreased in the model group (P