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Aims To study the effects of clenbuterol on anoxia/reoxygenation( A/R) injury in neonatal Wistar rat cardiomyocytes and to explore whether its mecha-nism is related to reperfusion injury salvage kinase ( RISK) or not. Methods The cultured primary neo-natal cardiomyocytes were randomly divided into eight groups: ①normal culture group; ②anoxia/reoxygen-ation( A/R) group;③ clenbuterol ( 1 μmol · L-1 ) +A/R;④ICI118,551(10 μmol·L-1) + clenbuterol ( 1 μmol · L-1 ) + A/R; ⑤Metoprolol ( 10μmol · L-1 ) + clenbuterol(1μmol·L-1 ) + A/R group;⑥Metoprolol ( 10 μmol · L-1 ) + A/R group; ⑦PD98059 ( 20 μmol · L-1 ) + clenbuterol ( 1 μmol · L-1 ) + A/R group;⑧ LY294002(10 μmol·L-1 ) +clenbuterol(1 μmol · L-1 ) + A/R group. Cell via-bility was determined by the conventional MTT reduc-tion assay. The content of LDH in cultured medium was measured with colorimetry. Cardiomyocyte apopto-sis was determined by Hoechst33342 . Intracellular re-active species( ROS) were monitored by the fluorescent DCFH-DA. Total ERK2 and phosphorylated ERK were detected by western blot. Results Compared with A/R group, clenbuterol significantly increased vaibility of cells, reduced LDH release, lowered the rate of apop-tosis and ROS production. When addedβ2 receptor an-tagonist ICI118 , 551 , PI3 K inhibitor LY294002 and ERK inhibitor PD98059 , the effects of clenbuterol a-bove were inhibited; but β1 receptor antagonist Meto-prolol protected the cardiomyocytes from A/R injury, as evidenced by decreased LDH release and increased cell viability. There were no synergistic effects in the combined use of clenbuterol and Metoprolol. Conclu-sion clenbuterol exerts cardioprotective effects against A/R injury by inhibiting oxidative stress and apopto-sis. The protection of clenbuterol is inhibited by ICI118 , 551 , LY294002 and PD98059 . clenbuterol protects cardiomyocytes against A/R injury via RISK pathway by activation of β2 receptor.
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Objective To investigate the protective effects of 3-n-butylphthalide (dl-NBP) on the cognitive dysfunction of chronic cerebral ischemic rats and its mechanism.Methods Old chronic cerebral ischemic rats (15 months) were modelized with ligating bilateral common carotid arteries for three months.Model rats were divided into four groups:sham,model,NBP 30 and 120 mg · kg-1 groups.The former and the latter two groups were administered vegetable oil and NBP for 45 days,respectively.Then,the cognitive function was measured in rats with Morris water maze.Meanwhile,the activities of superoxide dismutase (SOD),choline acetyltransferase (ChAT),true choline esterase (TChE),and the malondialdehyde (MDA) levels in brain cortex and hippocampus were detected with biochemical methods.Results During the five days of Morris water maze,the change of escape latency was from (57.7±3.8) s to (30.5±17.1) s in low dose of NBP group,and from (58.4±1.8) s to (28.9±11.3) s in high dose of NBP group as compared with no change from 60s to 60s in model group.Significant differences were found in escape latency between NBP's and model groups(P＜0.05 or 0.01).In spatial exploratory test,the time percentages spent in the platformquadrant were increased obviously in low and high doses of NBP [(26.0±6.9) ％ and (27.3±5.3) ％,respectively,P＜0.05],compared with that of model group.The SOD activity was obviously reduced in cortices of high dose of NBP group [(112.3 ± 7.6) U/mg protein] compared with that (134.6 ± 13.9) U/mg protein of model group (P＜0.01).The MDA contents were significantly reduced in cortices of low and high doses of NBP (2.39±0.31) nmol/mg protein and (1.56±0.19) nmol/mg protein,compared with that of model group (P＜0.01).The MDA contents in hippocampi of low and high doses of NBP [(0.71±0.10) nmol/mg protein and (0.83±0.05) nmol/mg protein] were also decreased significantly,compared with that of model group (P＜0.01).The ChAT level in cortex of high dose of NBP was increased significantly [(1615 ± 100) U/g protein,P＜0.05].The ChAT level in hippocampi of two doses of NBP also increased significantly [(1746±204) U/g protein and (1697± 117) U/g protein,P＜0.05].Conclusions NBP may improve cognition damage of chronic cerebral ischemic rats by ameliorating oxidative stress lesion and enhancing the activity of cholinergic nerve in brain tissue.
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ObjectiveTo perform pharmacology problem-based learning (PBL) and evaluate its effects.MethodsPBL was performed for the clinical medicine class of grade 2007 and the satisfactory degree of students to teaching effects was observed with questionnaire. Results The students thought that PBL teaching had substantial contents and proper schedule and increased learning interest. Students' participating degree, mutual communication and controlling discussion procedure were fine,which reached the expected learning objective. ConclusionsThe effects of PBL teaching were excellent and most of our students could accept it.
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Objective To investigate the effects of berberine on interleuk-1β( IL-1β) and tumor necrosis factor-α( TNF-α) and high-sensitivity C-reactive protein ( hs-CRP ) in diabetes rats induced by Streptozotocin ( STZ) , to explore the possible mechanisms of berberine on diabetic peripheral neuropathy . Methods Adult male SD rats were randomly divided into 4 groups:normal group , diabetic peripheral neu-ropathy group, berberine (100 mg/kg) group, berberine (187.5 mg/kg) group.The diabetic rat modes were i.p.injected with 1%STZ for two weeks, the rats were treated for 8 weeks respectively with berber-ine.The contents of IL-1βand TNF-αand hs-CRP in the serum and sciatic nerve were determined respec-tively by ELISA .Results The concentration of IL-1βand TNF-αand hs-CRP dropped obviously compared to DPN group ( P <0.05 ) .Conclusion It is suggested that berberine could possess the functions of de-creasing inflammatory mediator , antagonizing inflammatory reaction .Its therapeutic mechanism might be correlated with the improvement of inflammatory condition of diabetic rats ,and the promotion of sensitivity of insulin signal transduction in target tissues .
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BACKGROUND: Dihydrolycorine (DL) can inhibit the peripheral release of catecholamine from sympathetic nerve ending and block α, β adrenalinergic receptor. It has multiple pharmacological actions, such as vascular dilation, hypotension, anti-hypoglycemia and anti-ischemia.OBJECTIVE: To investigate the selective effect of DL on basilar artery,thoracic aorta and ventricular papillary muscle of rabbit by means of observing the vasoconstriction induced by noradrenaline bitartrate and KCl.DESIGN: Observation of comparative experiment.SETTING: Pharmacological Department of Yunyang Medical College.MATERIALS: This study was carried out at Pharmacological Department of Yunyang Medical College between March and July 2001, and 46 adult healthy New Zealand rabbits were selected.METHODS: New Zealand rabbits were put to death by intravenous injection of 10 mL air from the vein of aural edge, and soon after death, brain,thoracic aorta and heart were obtained. Basilar artery and thoracic aorta was linked into 4.0-5.0 mm vascular rings; meanwhile, ventricular papillary muscle were separated and connected with tension transducer. Obserdose of noradrenaline bitartrate or KCl: Sub-maximal constriction of thoracic aorta was induced by 0.1 mmol/L noradrenaline bitartrate or W60 mmol/L KCl, and when constriction curve became stable, DL or nimodipine of different dosage was added. Basilar artery was exposed to 0.1 mmol/L noradrenaline bitartrate or 60 mol/L KCl, and rinsing fluid was changed once every 20 minutes and thrice in all when vasocontratcion reached the peak level, then different dosage of DL or nimodipine was added 20 minutes later, and the changes of vasoconstriction curve due to administration of single dose of noradrenaline bitartrate or KCl were obconstriction of ventricular papillary muscular induced by electro-stimulation: Electro-stimulation was used to stimulate the ventricle papillary muscular synchronized constriction with the frequency of once per second,wavelength of 3 ms and threshold voltage of 120%; when constriction curve became stable, DL or nimodipine was administered in a accumulative way.ence of DL or nimodipine on the half-effective concentration of noradrenaline bitartrate or KCl that contributed to the vascular ring constriction of rabbit.RESULTS: Basilar artery, thoracic aorta and ventricular papillary muscle Resting tension of basilar artery was increased by DL but decreased by niof basilar artery and thoracic aorta induced by noradrenaline bitartrate and KCl can be relaxed by DL in a dose dependant manner, and the half-effective concentration was (6.69±3.12)×10-4, (3.41±1.52)×10-3mmol/L for basilar artery, and (1.49±0.59)×10-3, (2.91±0.99)×10-3 mmol/L for thoracic aorta, displaying stronger inhibition on the constriction of basilar artery induced by noradrenaline bitartrate than on the contraction induced by KCl.On the contrary, nimodipine showed stronger depression on KCl-induced constriction than on the constriction induced by noradrenaline bitartrate.ventricle papillary muscular induced by electro-stimulation in a dose-dependant manner, and the half-effective concentration of DL on the contraction of ventricle papillary muscle induced by electro-stimulation was significantly higher than that induced by noradrenaline bitartrate.CONCLUSION: DL displays obvious selective effect on basilar artery of rabbit, the possible existence of constrictive α1 receptor subtype and dilating β receptor on basilar artery might be correlated with the selective function of DL, which benefit, for the improvement of blood supply in the ischemic region.
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Aim To investigate effects of 1,25-(OH)2D3 on the differentiation of MGC-803 cells.Methods MGC-803 cells were treated by 1,25-(OH)2D3(10-6、10-5、10-4 mmol?L-1),and the rate of growth suppression was evaluated by 3-(4,5-dimethylthiazole-2-yl)-2,5-diphenyl tetrazolium bromide(MTT) assay.Plate clone formation assay was carried out to detect the phenotypes of colony formation.FACS analysis was used to analyze the cell cycle.The activity of telomerase was examined by telomeric repeat amplification protocol(TRAP) PCR-silver staining.Results 1,25-(OH)2D3 showed significant inhibitory effect on growth of these gastric carcinoma cells at 24,48,72 and 96 h.Treated with 1,25-(OH)2D3 for 48 h,cell cycle showed G0/G1 phase arrest,and the activity of telomerase was inhibited significantly.The colony-forming rate was reduced drastically(P
