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1.
目的:探讨环腺苷酸(cAMP)对大鼠神经胶质瘤细胞C6的诱导分化作用。方珐:C6细胞经不同浓度的cAMP诱导后,应用MTT分析法、软琼脂克隆形成、电镜检测、流式细胞仪、GFAP免疫组化染色及TUNNEL染色等法,检测C6细胞的分化及凋亡情况。结果:0.2mmol/L cAMP即可诱导C6细胞分化,表现为增殖抑制、细胞突起增长增多、G1期阻滞、GFAP高阳性表达、线粒体增多.细胞核变小等。且有浓度依赖关系,10mmol/L cAMP可诱导出现凋亡。结论:cAMP可明显抑制C6细胞增殖、诱导细胞分化甚至凋亡。  相似文献   

2.
将32例妊娠高血压综合征(PIH)患者随机分为PIH组(15例)和青心酮(DHAP)治疗组(17例),同时取相应年龄未孕妇女(16例)及正常孕妇(15例)作为对照组。采用放射免疫技术测定各组外周血(母血)、脐静脉血(胎血)的心纳素(ANP)、环磷酸腺苷(cAMP)、环磷酸鸟苷(cGMP)水平。结果发现:正常孕妇血浆ANP及cAMP、cGMP水平较未孕者略有增高,但无统计学意义(P>0.05);而 PIH患者母血ANP及cGMP较未孕或正常孕妇明显增高(P相似文献   

3.
Summary:To evaluate the changes of 3',5'-cyclic adenosine monophosphate(cAMP),thromboxane A_2(TXA_2)and prostacyclin(PGI_2)in cerebrospinal fluid(CSF)in the asphyxiated newborn andexplore their roles in hypoxic-ischamic brain damage(HIBD).Thirty-six full term newborns were di-vided into 3 groups,including 12 with moderate-severe hypoxic-ischaemic encephalopathy(HIE),13with mild HIE,11 without HIE(control group).The levels of cAMP,TXB_2(TXA_2 metabolite)and6-keto-PGF_(1α)(PGI_2 metabolite)in CSF and plasma were measured 36—72h after birth by RIA.andthe concentrations were expressed as nM/L(cAMP),ng/L(TXB_2 and 6-keto-PGF_(1α)).The infantswere followed-up at 6 and 12 month of age and Mental Development Index(MDI)and PsychomotorDevelopment Index(PDI)were measured using Bayley Scales of Infant Development(BSID).TheCSF cAMP level in moderate-severe HIE group was 8.60±2.40,significantly lower than that of themild HIE group(14.83±2.84)and the control group(24.43±2.39)(for both P<0.01).The lev-els of TXB_  相似文献   

4.
用外源性3′,5′环腺苷酸(3′,5′cAMP)对人肺腺癌细胞系的连续作用,观察到癌细胞的增殖受到明显抑制,同时观察到在3′,5′cAMP作用下的癌细胞在裸小鼠体内移植瘤生长受到一定的抑制,但7周抑制作用基本消失。  相似文献   

5.
To confirm the existence of heme oxygenase (HO)-carbon monoxide (CO)- cyclic guanosine monophosphate (cGMP) pathway in the cultured human trabecular meshwork cells (HT-MCs) in vitro, and to evaluate the inductive role of heroin on this pathway, HTMCs of the third to fourth generation were cultured in vitro. Reverse transcripase-polymerase chain reaction (RT-PCR) was employed for detection of HO-1 and HO-2 mRNA. Immunohistochemical staining was used to detect HO-1 and HO-2 proteins. Hemin was added into the culture solution. The HO-1 mRNA levels were quantified by RT-PCR. The relative amount of carbon monoxide released into the media was measured with the quantifying carbon monoxide hemoglobin (HbCO) by spectrophotometry.Radioimmunoassay was used to determine changes of cGMP in HTMCs. The results showed that cultured cells had the specific characteristics of HTMCs. Both HO-1 and HO-2 genes were expressed in HTMCs, as well as HO-1 and HO-2 proteins in HTMCs. Hemin induced HO-1 mRNA,HbCO and cGMP in a dose-dependent manner. In conclusion, HO-CO-cGMP pathway exists in the cultured HTMCs and can be induced by hemin. Pharmacological stimulation of HO-CO-cGMP pathway may constitute a novel therapeutic approach to rescuing glaucoma.  相似文献   

6.
目的:探讨地塞米松对环腺苷酸(cAMP)诱导C6胶质瘤细胞分化的影响。方法:应用地塞米松和RU486单独或共同与cAMP作用于C6胶质瘤细胞,通过Western blotting检测胶质细胞分化标志蛋白(glial fibrillary acidic protein,GFAP)表达变化,光镜观察细胞形态学变化;通过Western blotting和细胞免疫荧光观察CREB磷酸化水平。结果:地塞米松与cAMP共作用于C6胶质瘤细胞48h,抑制GFAP表达和细胞形态改变;糖皮质受体抑制剂RU486逆转地塞米松的作用;地塞米松抑制cAMP诱导的CREB磷酸化。结论:地塞米松通过抑制CREB磷酸化逆转cAMP诱导的胶质细胞分化。  相似文献   

7.
目的 藉离子霉素提高细胞内游离钙浓度([C^2 ]i),观察其对急性白血病HL-60细胞内环核苷酸水平的影响。方法 在IBMX抑制磷酸二酯酶作用后加入离子氯素提高[C^2 ]i,比较[C^2 ]i升高对静息水平和肾上腺素刺激水平的HL-60细胞内cAMP,cGMP水平的影响,cAMP,cGMP水平以环核苷酸的累积量表示。结果 [C^2 ]i升高可使静息和肾上腺素刺激水平的cAMP累积量明显降低,cGMP累只量无明显改变,[C^2 ]i升高对硒诱导分化后的HL-60细胞环核苷酸的影响同分化前一致。结论 [C^2 ]i升高能够降低HL-60细胞内cAMP水平,对cGMP水平无影响,这种作用不因细胞分化而改变。  相似文献   

8.
本实验采用沙土鼠双侧颈总动脉结扎模型观察人参二醇皂甙(PDS)对缺血-再灌注脑过氧化脂质(LPO)和环磷酸腺苷(cAMP)含量的影响。结果发现PDS200mg/kg缺血前30minip可减少LPO生成,抑制CAMP下降,提示PDS对脑缺血-再灌注损伤的保护作用可能与抑制脂质过氧化反应,改善cAMP代谢有关。  相似文献   

9.
创伤小鼠淋巴细胞内环磷酸腺苷,环磷酸鸟苷的变化   总被引:1,自引:1,他引:0  
用小鼠闭合伤、截肢伤及烧伤模型,观察创伤后4d小鼠脾细胞、胸腺细胞、肠系膜淋巴结细胞内环磷酸腺苷(cAMP)、环磷酸鸟苷(cGMP)的变化。结果显示:创伤后三种类型的淋巴细胞在静息状态或经ConA刺激时的cAMP水平增高,cGMP水平下降,cAMP/cGMP比值增加。创伤后血清、巨噬细胞、Ts细胞在体外可明显提高正常小鼠脾细胞内cAMP水平,降低其cGMP水平。去除创伤小鼠脾细胞中的巨噬细胞、Ts  相似文献   

10.
目的:探讨5种常用化疗药物对人胃癌细胞生长的抑制作用。方法:选用不同浓度的化疗药物采用体外短期培养法,结合H3-TdR掺入技术测定其对新鲜人胃癌标本细胞生长的抑制率。结果:5种化疗药物对19例胃癌细胞的抑制率从高到低顺序为:5-FU、VP-16、MTX、MMC、ADM。其抑制率有随药物浓度提高而增高的趋势,各个体间的抑制率不同。药物中浓度对分化不良型(低分化及印戒细胞癌)的敏感性明显高于分化良好型(高,中分化型)。结论:化疗药物对不同个体胃癌细胞体外抑制率有显著差异,体外检测化疗药物的敏感性可为临床化疗提供指导。  相似文献   

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