BACKGROUND:Prostate is susceptible to infection and pro-inflammatory agents in a man's whole life. Chronic inflammation might play important roles in the development and progression of prostate cancer. Mesenchymal stem cells (MSCs) are often recruited to the tumor microenvironment due to local inflammation. We have asked whether stimulation of MSCs by pro-inflammatory cytokines could promote prostate tumor growth. The current study investigated the possible involvement of MSCs stimulated by pro-inflammatory cytokines in promotion and angiogenesis of prostate cancer through relative pathway in vitro and in vivo.METHODS:A syngeneic mouse model of C57 was established. The murine prostate cancer cells (RM-1) mixing with MSCs treated with tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ) or vehicle were subcutaneously injected into C57 mice. Tumor volume of C57 mouse model was estimated and serum level of platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF) was test by Enzyme-linked Immunosorbent Assay (ELISA). A hen egg test-chorioallantoic membrane (HET-CAM) assay was applied to test the effect of conditioned media of stimulated MSCs in chorioallantoic membrane angiogenesis. Short interfering RNA (siRNA) knocked down either hypoxia-inducible factor-1alpha (HIF-1α) or nuclear factor-erythroid-2-related factor 2 (NRF2) were employed. mRNA of PDGF and VEGF in MSCs, as well as NRF2 and HIF-1α was test by Real time polymerase chain reaction (PCR) analyses. Protein expression levels of PDGF and VEGF from conditioned medium, NRF2, HIF-1α, as well as PDGF and VEGF in MSCs were detected by Western blot analysis.RESULTS:MSCs treated with TNF-α and IFN-γ promote tumor growth in C57 syngeneic mouse model, correlating with increased serum level of PDGF, VEGF. HET-CAM assay shows the angiogenic effect of conditioned medium of MSCs pre-treated with the pro-inflammatory cytokines. mRNA and protein levels of two pro-angiogenic factors (PDGF and VEGF) and key hypoxia regulators (HIF-1α and NRF2) in MSCs were induced after MSCs' pretreatment. siRNA knockdown either HIF-1α or NRF2 results reduction of PDGF and VEGF expression.CONCLUSIONS:MSCs stimulated by pro-inflammatory cytokines increase the expression of PDGF and VEGF via the NRF2-HIF-1α pathway and accelerate prostate cancer growth in mice.

Mesenchymal stem cells (MSCs) play an important role in the development of human prostate cancer (PCa). However, the role of MSCs in the transformation of androgen-dependent human PCa cells into androgen-independent manner has been poorly understood. In this study, we investigated the underlying mechanism of MSCs in promoting PCa cells from androgen-dependent into androgen-independent manner. Firstly, we demonstrated that MSCs could affect the transformation of androgen-dependent human PCa cells into androgen-independent manner in vivo and in vitro. Then we found a substantial expression of TGF-β in MSCs. TGF-β blockade could significantly inhibit the promotive function of MSCs in PCa cells. Besides that, we also demonstrated androgen might inhibit the expression of TGF-β in MSCs. Furthermore, we found that either overexpression of SSEA-4 or the number of SSEA-4 positive MSCs in PCa tissues was associated with a shorter cancer-free survival interval (CFSI) and a worse overall survival (OS). Our results suggest that androgen blockade treatment in clinical PCa therapy may elicit the expression of TGF-β in MSCs, which will result in the transformation of androgen-dependent human PCa cells into androgen-independent manner.

Radiotherapy has long been considered as the mainstay of treatment for nasopharyngeal carcinoma (NPC). However, locoregional recurrence or distant metastasis may occur in some patients due to the radiation resistance of cancer cells. Autophagy plays a vital role in protecting cells against radiation. However, the mechanism of autophagy in radiation therapy remains obscure. In the present study, we demonstrated that suppression of autophagy related 5 (Atg5) aggravated ionizing radiation (IR)-induced DNA damage and apoptosis in human NPC cells without accelerating the cell cycle, whereas regulation of the cell cycle has been widely regarded as the most important determinant of IR sensitivity. Further study showed that inhibition of autophagy suppressed the mRNA expression of Rad51, a key protein of homologous recombination that has been demonstrated to play a critical role in the repair of DNA double-strand breaks induced by radiation. Moreover, suppression of Atg5 had no impact on the radiosensitivity when cells were pre-treated by the Rad51 inhibitor, and the enhanced radiosensitivity by Atg5 suppression was reversed by overexpression of Rad51 in human NPC cells. Our results suggest that inhibition of autophagy enhances the susceptibility of NPC cells to radiation by reducing Rad51 expression. Therefore, Rad51 targeted therapy may be investigated as a potential novel agent for the adjuvant treatment of traditional radiation of NPC.

Objective To explore the relationship between mesenchymal stem cells with prostate cancer growth in mice , in order to find new targets for the treatment of prostate cancer .Methods C57BL/6 wt‐mice received lethal irradiation ,ac‐cepted mixed EGFP transgenic C57BL/6 mouse MSCs and wild‐type mice bone marrow cells .Then subcutaneous tumor model of RM‐1 prostate cancer cell was established and the growth of prostate cancer was detected .EGFP‐MSCs cells in prostate cancer tissues were observed and detected with fluorescence microscopy imaging techniques and flow cytometry .Results Af‐ter RM‐1 prostate cancer cells were subcutaneous inoculated ,the tumor growth rate of the experimental group receiving intra‐venous injection of MSCs ,was higher than that of the control group which received NS .Tumor weights were (3 .730 ± 0 .632) g and (2 .019 ± 0 .254)g respectively ,(P< 0 .05) .Either endogenous MSCs from bone marrow transplantation or exogenous MSCs from direct intravenous injection could be detected in prostate cancer tissues .Conclusion Endogenous and exogenous MSCs cells can be chemotacticly recruited to prostate cancer to promote cancer growth .

Aim To study the effects of chronic morphine treatment on the expression of phosphorylated cAMP response element binding protein(pCREB) and CREB mRNA in sympathetic ganglia,superior cervical ganglia(SCG) of rats.Methods The Wistar rats were randomly divided into 4 groups,namely control, morphine acute,morphine dependent and morphine withdrawal group.The expression of pCREB and CREB mRNA in SCG was detected by means of immunohistochemistry and RT-PCR respectively.Results(1) The content of pCREB in SCG of morphine-acute group was lower than that of control group(P0.05).(2) The content of pCREB in SCG of morphine dependent group returned to the level of control group with an increasing tendency(compared with control,P0.05;compared with morphine-acute,P0.01).(3) Compared with control group,the content of pCREB in SCG of morphine withdrawal group was increased(P0.01).(4) The expressive level of CREB mRNA in SCG was not significantly changed in each group(P0.05).Conclusion There is an up-regulation of pCREB in sympathetic ganglia of chronic morphine treated rats.

Objective:To observe the effect of GM1 on nitric oxide synthase(NOS),including constitutive nitric oxide synthase(cNOS) and induced nitric oxide synthase(iNOS) following cerebral damage after CPB in rats.Methods: SPF-class adult male SD rats were randomly divided into CPB,CPB+GM1,transfusion,and sham-operated groups.After establishing a rat model of cardiopulmonary bypass,GM1 with 20 mg/kg was added to the priming solution.All rats were anesthetized to collect the whole cerebral tissues for detecting the activity of cNOS,iNOS and NO content after 24 hours.Results: Compared with the control group,the level of iNOS and NO increased significantly(P<0.05),while the cNOS activity decreased significantly(P<0.05) in the CPB group.GM1 administration obviously descended the activity of iNOS and NO and increased the cNOS activity.Conclusion: The rise of iNOS activity could correlate closely with brain injury after CPB,and GM1 could reduce iNOS activity and NO content.GM1 has the effect of brain protection against the neurotoxicity of NO.

目的:研究三七总皂苷(Panax notoginseng saponins,PNS)对海马脑片CA1区锥体神经元兴奋性突触活动的作用和机理.方法:采用"盲法"全细胞膜片钳技术,记录PNS(0.05～0.4 g/L)对3～4周雄性 wistar大鼠海马脑片(400 μm)CA1区兴奋性突触后电流(excitatory post synaptic currents,EPSCs)和自发的微小兴奋性突触后电流(miniature excitatory post synaptic currents,mEPSCs)幅度及频率的影响.结果:0.1～0.4 g/L PNS显著抑制海马脑片CA1区EPSCs(P<0.05);0.05～0.4 g/LPNS可明显增加CA1区锥体神经元自发mEPSCs的产生频率,但并不影响mEPSCs的幅度.结论:PNS可作用于突触前位点对海马神经元兴奋性突触活动产生调节作用,PNS增加mEPSCs频率的作用可能与促进突触前膜nAChR的激动有关,这可能是其调节海马神经元的兴奋性进而发挥益智作用的机制之一;PNS对EPSCs和mEPSCs的不同作用说明PNS是选择性抑制膜去极化所诱发的递质释放过程,PNS的这种选择性作用对于其发挥神经保护作用十分有利.

Aim To study the effects of chronic morphine treatment on the contents of cAMP and cGMP in sympathetic ganglia,superior cervical ganglia(SCG) of rats.Methods The chronic morphine dependent model of rats was established by subcutaneous injection of morphine in gradually increasing doses for 5 days,the dependence and the tolerance of the model was estimated by naloxone precipitation test and 55℃ tail-flick trail test respectively.The contents of cAMP and cGMP in SCG were detected by means of 125I radioimmunoassay.Results ① Compared with control group,the content of cAMP in SCG of morphine-acute group rats was descended(P0.05);② The content of cAMP in SCG of morphine dependent group rats was returned to the level of control group with an increased tendency(compared with control,P0.05;compared with morphine-acute,P0.05).③ Compared with control group,the content of cAMP in SCG of morphine withdrawal group rats was increased(P0.05);④ The content of cGMP in SCG was not significantly changed in every group(P0.05).Conclusion There was an up-regulation of cAMP in sympathetic ganglia of chronic morphine treated rats.

Objective To investigate the effects of Panax notoginseng saponins(PNS)on both the excitatory and inhibitory synaptic transmission in the pyramidal neurons in hippocampal CA1 region of rats.Methods Wistar male rats(3—4 weeks)were killed by cervical dislocation and hippocampal slices(400 μm)were prepared,blind whole-cell voltage-clamp recordings were performed on the CA1 pyramidal cells in hippocampal slices to examine and analyze the effects of PNS(0.05—0.4 g/L)on CA1 afferent fiber-evoked excitatory postsynaptic currents(EPSCs)and inhibitory postsynaptic currents(IPSCs),respectively.Moreover,the Schaffer collateral/commissural pathway was stimulated with paired pulses(interpulse interval was 50 ms)and the paired-pulse facilitation(PPF)was analyzed by EPSC2/EPSC1(P2/P1)ratio.Results PNS(0.1—0.4 g/L)significantly depressed amplitude of EPSCs in neurons in the hippocampal CA1 region(P0.05).The P2/P1 ratio was markedly increased after PNS application(P0.05).But amplitude of IPSCs had no significant changes(P0.05).Conclusion The inhibitory effect of PNS on EPSCs in hippocampal CA1 pyramidal neurons is not due to the reinforcement of the inhibiting interneurons.It may be a result of direct inhibition on excitatory synaptic transmission.The increasing of P2/P1 ratio after PNS application suggests that PNS depresses the excitatory synaptic transmission by presynaptic mechanism.

Panax notoginseng saponins (PNS) are very important extracts from roots of medicinal herb Sanchi Ginseng which is highly regarded in China for its therapeutic ability to meliorate blood-circulation, anti-anoxia, improve memory, and anti-caducity effects. In this study, we used blind whole-cell voltage-clamp recordings to detect the effects of PNS on long-term potentiation (LTP) in the CA1 region of the hippocampus, and investigated the electrophysiological mechanisms underlying potentiating effects of PNS on learning and memory. Wistar rats (3-4 weeks) were decapitated and hippocampal slices (400 microm thick) were cut coronally. Excitatory postsynaptic currents (EPSCs) were recorded by patch clamp technique in whole-cell configuration. The Schaffer collateral/commissural pathway was stimulated by high frequency stimulation (HFS: 100 Hz) pulses to induce LTP. The findings showed that 0.1 - 0.4 g x L(-1) PNS significantly depressed the amplitude of EPSCs (P < 0.05) and had no facilitative effects on LTP of pyramidal neurons located in the CA1 region. PNS in the concentrations of 0.04 - 0.05 g x L(-1) did not appreciably affect the amplitude of EPSCs (P > 0.05) but markedly increased the amplitude of LTP (P < 0.05). In conclusion, 0.04 - 0.05 g x L(-1) PNS could facilitate LTP in the CA1 region of the rat hippocampus and it is reasonable to suggest that this action may contribute to its potentiating effects on learning and memory.

BACKGROUND: Panax notoginseng saponins (PNS) could significantly improve the learning and memory ability of rats, but its influence to peripheral nervous system still needs further investigation.OBJECTIVE: To observe the effects of PNS on the fast-excitatory postsynaptic potential (f-EPSP) in stellate ganglion (SG) of rats.DESIGN: Observation and controlled trial.SETTING: Pharmacological Laboratory of Guangxi Medical University.MATERIALS: The experiment was carried out at the Pharmacological Laboratory of the Experimental Center of Guangxi Medical University from January 2005 to February 2006. Thirty healthy male SD rats of clean grade and (220±20) g, provided by the Experimental Animal Center of Guangxi Medical University; SEN-7203 digital three track strip stimulator, microelectrode amplifier (MEZ8301, Japan NIHON KOHDEN COMPANY); glass microelectrode puller, and microelectrode manipulator, both the products of Narishige Company, Japan; PNS, provided by Kunming Jacobson Pharmaceutical Co., Ltd, and acetylchloride chline (Ach), the product of Sigma, U.S.A.METHODS: After the animals were executed acutely, their chest wall was opened to isolate SG rapidly under microscope, which was transferred to the perfusion chamber, and fixed with wire needles after peeling the connective tissue membrane. The ganglia were perfused continuously with the mixture of volume fraction 0.95 O2 and 0.05 CO2 plus Krebs solution with pH (7.4±0.05). Meanwhile, 0.08-0.16 g/L PNS was employed to perfuse and culture SG.①The glass microelectrode filled with 3 mmol/L KCI was used to puncture the isolated SG and record the amplitude and duration of depolarizing reaction of postsynaptic membrane.②PNS with the maximum concentration of 0.16 g/L, which could inhibit the f-EPSPs, was perfused to observe the effect of PNS on the amplitude and duration of depolarizing reaction of postsynaptic membrane induced by exogenous Ach (1 mmol/L, 1 minute).③PNS with the maximum concentration of 0.16 g/L, which could inhibit the f-EPSPs, was perfused to observe the effect of PNS on membrane resistance and membrane potential.MAIN OUTCOME MEASURES:①Amplitude of depolarizing reaction of postsynaptic membrane; ②Effect of PNS on the amplitude and duration of depolarizing reaction of postsynaptic membrane induced by exogenous Ach, and membrane resistance and membrane potential.RESULTS: Thirty rats were involved in the result analysis. ①PNS ranged 0.08 to 0.16 g/L could reversibly depress the f-EPSPs amplitude of, or change the forward active potential into f-EPSP; the higher the concentration of PNS, the more obvious the inhibition was. The depression appeared in 3-10 minutes after PNS perfusion, and the effect reached the peak at 0.16 g/L; f-EPSP was decreased evidently in 3 to 4 minutes. The inhibition nearly recovered to the control level after washing the ganglia with Krebs solution for 15 to 20 minutes. ②Effect of PNS on exogenous ACh-induced depolarization: The amplitude and duration of the Ach-induced depolarization did not significantly change before and 5 minutes after 0.16 g/L PNS perfusion [before: (15.5±2.4) mV, (256.1±21.5) seconds; after: (14.3±1.9) mV, (228.6±24.5) seconds, P＞0.05].③Effects of PNS on membrane potential and membrane resistance: The mean membrane potential and membrane resistance were not significantly changed after PNS perfusion [before:-(55.5±12.1) mV, (53.9±5.1) MΩ; after: -(54.3±10.4) mV, (55.1±4.8)MΩ, P＞0.05].CONCLUSION: PNS could reversibly depress the fast-excitatory postsynaptic potential in stellate ganglion of rats by presynaptic mechanism.

BACKGROUND: The rare earth elements (Res) have multiple bio-activities and some extent neurotoxicity, Because of their distinct physical and chemical properties. The studies on neuromuscular junction and sympathet ic ganglia have shown that some Res, such as lanthanum(La), gadolinium (Gd),etc, exert considerable effects on synaptic transmission, but the effects and mechanism of Samarium on synaptic transmission are still unknown.OBJECTIVE: To investigate the effects and impossible mechanism of Samarium Chloride (SmCl3) on the nicotinic transmission in the isolated sympathetic ganglia, superior cervical ganglion (SCG) of rats.DESIGN: Controlled experimental study based on cells.SETTING: Department of Pharmacology, Guangxi Medical University. MATERIALS: Totally 40 adult Wistar rats (weighing 250-300 g) of either sex, provided by the Experimental Animal Center of Guangxi Medical University, were used in this study. SmCl3 was made by the chlorination of Samarium Oxide with purity 99.5% and relative molecule mass 348.7, presented by Professor Liu Da-yuan, Guangxi Medical University. Acetylcholine chloride (Ach) and carbachol (Carb) were purchased from Sigma.METHODS: The experiment was completed at the neuropharmacology lab of the experimental center of Guangxi Medical University from September 2001 to December 2002. After sacrificing animals by acute exsanguination,SCG together with their preganglionic nerve trunks were isolated rapidly,then transferred to the recording chamber, the preganglionic nerve trunk was drawn into a suction electrode for orthodromic stimulation. The ganglia were superfused continuously with a Krebs solution, saturated with 950 mL/L 02 and 5mL/L CO2, pH 7.4±0.05, (34±0.5) ℃.The fiber containing glass microelectrodes filled with 3 mol/L KC1 (30-60 MΩ tip resistance) were used to impaled cells and do intracellular recording. The fast excitatory postsynaptic potentials (FEPSPs) were evoked in SCG neurons by single pulse stimulations (0.2-0.5 Hz, 0.5-1.0 ms, 2-10 V)on preganglionic nerve trunk. The remarkable membrane depolarization would be recorded in SCG neurons by superfusing ganglia with exogenous Ach (0.1 mmol/L) or Carb(0.1 mmol/L) for 30-60 s. The effects of 1×(10-7-10-4) mol/L SmCl3 on FEPSPs, membrane potentials, membrane resistance, exogenous Ach and Carb-induced membrane depolarization of SCG neurons were investigated in this experiment.The effects of SmCl3 on the facilitation of high Ca2+ (10 mmol/L ) on FEPSPs were also be observed, namely, first superfusing the ganglia with high Ca2+ (10 mmol/L)to facilitate FEPSPs, then superfusing the ganglia with Ca2+(10 mmol/L)contained SmCl3. All the drugs were solved in Krebs solution or improved Krebs solution and applied to ganglia by superfusion in known concentration.The bioelectricity difference before and after the drug superfusion were analyzed by paired Student's t test.MAIN OUTCOME MESURES: ①Effects of SmCl3 on FEPSPs.②Effects of SmCl3 on membrane potentials and membrane resistances. ③Effects of SmCl3 on exogenous Ach and Carb-induced membrane depolarization. ④Effects of SmCl3 on the facilitation of high Ca2+ (10 mmol/L ) on FEPSPs.RESULTS: ① 1 ×(10-7-10-4)mol/L SmCl3 could reversibly depressed the FEPSPs of rats SCG neurons [the amplitude inhibitory percentage of FEPSPs of l×10-4, 1×10-5, 1×10-6, 1×107 mol/L SmCl3 was (49.78±13.85)%(n=20),(39.05±4.05)%(n=10),(29.83±9.73)%(n=10)and (16.30±2.16)%(n=10)respectively (P ＜ 0.05-0.01)].1×10-4 mol/L SmCl3 could chang Aps into FEPSPs (n=5).②The membrane depolarization induced by Ach (n=5) and Carb (n=7) were not significantly changed by 1×10-4 mol/L SmCl3(P ＞ 0.05).③The membrane potential and membrane resistance were not significantly altered by 1×(10-7-10-4)mol/L SmCl3(n=67), P ＞ 0.05. ④1×10-4 mol/L SmCl3 could antagonized the facilitation of high Ca2+ (10 mmol/L ) on FEPSPs (n=5), P ＜ 0.01.CONCLUSION: SmCl3 can depresses nicotinic transmission in rats sympathetic ganglia by presynaptic mechanisms, perhaps due to its inhibition on Ca2+ influx.

目的 以观察大鼠切口疼痛模型中皮下注射(sc)氯胺酮对外周交感神经节一氧化氮(NO)和一氧化氮合酶(NOS)的影响.方法雄性SD大鼠65只,行为学评分分组:分五组,每组5只:生理盐水组,氯胺酮组(5mg/kg组,10mg/kg组,2 0mg/kg组),吗啡组;NO和NOS测定分组:分五组,每组8只:正常组,生理盐水组,氯胺酮组(10mg/kg组,20mg/kg组),吗啡组.按Brennan法[1]制成切口疼痛模型,以累积疼痛评分和冷刺激评分确定疼痛行为.在给药后30min快速脱臼处死动物取交感神经节,用分光光度计测定NOS(总NOS和iNOS)活性,酶标仪测定NO含量.结果累积疼痛评分和冷刺激评分,氯胺酮组(10mg/kg组,20mg/kg组)、吗啡组均低于生理盐水组(P＜0.05).NO含量测定,氯胺酮组(10mg/kg组,2 0mg/kg组)、吗啡组均低于生理盐水组(P＜0.05).NOS活性测定,氯胺酮组(10mg/kg组,2 0mg/kg组)、吗啡组均低于生理盐水组(P＜0.05).但与正常组没有明显差别.结论在大鼠切口疼痛模型中,皮下注射不同剂量氯胺酮,其镇痛机制可能与降低外周交感神经系统NO含量和NOS活性有关。

Aim To study the relationship between theeffects of saponins of panax notoginseng(PNS)on fir-ing frequency and hyperpolarization potential in neu-rons.Methods Applieation of a depolarizing currentpulse to stellate ganglion(SG) neurons of rat evokedaction potentials(AP).These neurons were classifiedas phasic or tonic neurons on the basis of their firingpatterns.Then we investigated the effects of PNS on fir-ing pattern and frequency,after hyperpolarization po-tential(AHP) and fastexcitatory postsynaptic potential(f-EPSP) in high Ca2 +Krebs’solution of SG neuronsin rat.Results The firing frequency of tonic neuronswas reduced by PNS.At the concentration of0.12 ~0.16 g.L-1,PNS reversibly depressed AHP in a dosedependentmanner.And the aggrandizing action of highCa2 +on f-EPSP was antagonized by PNS.Conclusion PNS can reduce the firing frequency of rat SG neu-rons,but this action was not caused by reinforcement ofAHP potential.The restraining regulation of excitabili-ty of neurons by PNS may underlie its inhibitory actionon calcium influx.

In order to observe the analgesic effect of hypodermic injection of Ketamine in a rat model of incisional pain and the effect on Nitric Oxide(NO) and Nitricoxide synthase(NOS) in the cerebral cortex,eighty male SD rats weighing of(250±20)g were used in our experiment.These animals were equally divided into 10 groups.Among them,5 groups were used in ethology investigation of Saline,Ketamine(5mg/kg,10mg/kg,20mg/kg),Morphia;another 5 groups were used in NO/NOS measurements of normal control,Saline,Ketamine(10mg/kg,20mg/kg) and Morphia.According to the Brennan's method to build an incision pain model,cumulative pain score and cold stimulation score were utilized to assess pain behavior.The cerebral cortex was removed at 30min after administration to measure NO production and NOS(total NOS and iNOS) activity.Results indicated that the cumulative pain score and cold stimulation score were lower in Ketamine groups(10mg/kg group and 20mg/kg group)and Morphia group than Saline group(P0.05);and the NO production and the NOS activity in Ketamine groups(10mg/kg and 20mg/kg groups) and Morphia group were lower than Saline group(P0.05).It produces that the analgesic effect could be produced by hypodermic injection of different dosage Ketamine in a rat model of incisional pain.No and NOS may play an important role in the analgesic effect of the central nervous system.

新近研究发现,左心室肥厚可见于高血压的极早期,甚至少数高血压患者在血压升高前就存在室壁肥厚.这些资料表明左心室肥厚可由独立于血压之外的因素导致.越来越多的证据表明,左心室肥厚和神经体液内分泌因素密切相关.左心室肥厚作为心肌对心肌损伤及心脏超负荷的一种反应,反映了体内生长促进因子[如血管紧张素Ⅱ(AngⅡ)、细胞因子、生长因子、去甲肾上腺素、甲状腺素等]和生长抑制因子(如心钠素、缓激肽、前列腺素及NO等)之间效应的失衡.前者直接调节和促进心肌细胞生长,后者则可扩张血管、减轻心脏负荷、增加胶元降解,对抗AngⅡ等生长促进因子的作用.本文综述AngⅡ在左心室肥厚发病机制中的作用.

Aim To study effects of morphine tolerance and dependence on the fast excitatory synaptic transmission in sympathetic ganglia of rats.Methods The isolated sympathetic ganglia,superior cervical ganglia(SCG), were made from control and morphine tolerant and dependent rats respectively.Effects of morphine tolerance and dependence on the fast excitatory synaptic transmission in rat sympathetic ganglia were studied by means of intracellular recording technique.Results ① Morphine(0.1～1.0 mmol·L~(-1))reversibly inhibited the amplitude of the fast excitatory postsynaptic potentials(f-EPSPs) in SCG neurons of control rats.② Compared with control group,inhibitory effects of morphine(0.5 mmol·L~(-1) and 1.0 mmol·L~(-1)) on f-EPSPs in SCG neurons of morphine tolerant and dependent rats were obviously decreased;③ Naloxone(0.1 mmol·L~(-1)),which had no significantly effect on f-EPSPs in SCG neurons of control rats,could reversibly facilitate the amplitude of f-EPSPs in SCG neurons of morphine tolerant and dependent rats;④ No significant difference of RMP and Rm was founded between SCG neurons of control and morphine tolerant and dependent rats.Conclusion The morphine tolerant and dependent of the fast excitatory synaptic transmission in rat sympathetic ganglia has been formed in morphine tolerant and dependent rats.

目的:探讨三七总皂甙(PNS)对大鼠星状神经节快兴奋性突触后电位的影响及机制.方法:用细胞内生物电记录技术,测定PNS对大鼠星状神经节(SG)的快兴奋性突触后电位(f-EPSP)、膜电位、膜电阻及对外源性乙酰胆碱引起的膜除极化反应的影响.结果:PNS在0.10～0.1 6 g/L浓度范围内可使f-EPSP可逆性减小(P＜0.01),但对膜电位、膜电阻及外源性氯化乙酰胆碱(Ach)引起的膜除极反应均无显著的影响.结论:PNS对大鼠星状神经节f-EPSP有可逆性抑制作用,抑制是通过突触前机制产生.

目的:研究银杏叶提取物(EGb761)对离体大鼠颈上神经节烟碱传递的影响.方法:应用细胞内生物电记录技术观察了EGb761给药前后,离体大鼠颈上神经节f-EPSP的幅值、膜电位、膜电阻、Ach和Carb引起的膜除极化反应及高钙易化f-EPSP的幅值等指标的变化.结果:在10-6～10-3g/L浓度下,EGb761能可逆性地部分或完全地抑制快兴奋性突触后电位(f-EPSP),抑制作用在高钙溶液中仍然存在,但不影响外源性乙酰胆碱(Ach)和氨甲酰胆碱(Carb)引起的膜除极化反应;EGb761单独灌流对细胞膜电位、膜电阻无明显影响.结论:10-6～10-3g/L的EGb7611对离体大鼠颈上神经节突触烟碱传递的抑制作用与突触前机制有关,可能抑制了突触前膜的钙离子内流.

目的:研究三七总皂苷(PN S)对去甲肾上腺素(NE)诱导的新生大鼠心肌肥大的作用,并探讨其作用机制。方法:用NE诱导培养新生大鼠心肌细胞制作心肌肥大模型。经G iem sa染色后用图像分析仪测定细胞表面积,B rad ford法测细胞蛋白质含量,观察0.02、0.1、0.5 g.L-13个浓度的PN S对肥大心肌细胞的影响。结果:肥大组细胞表面积及蛋白质含量比对照组明显增加(P<0.01);PN S中、高剂量组与肥大组比较,细胞表面积及蛋白质含量均显著减少(P<0.01);低剂量PN S对细胞表面积及蛋白质含量无明显影响(P>0.05)。结论:PN S可浓度依赖性地拮抗NE诱导的大鼠心肌细胞的肥大反应。