After hypoxia, ischemia, or inlfammatory injuries to the central nervous system, the damaged cells release a large amount of adenosine triphosphate, which may cause secondary neuronal death. Autophagy is a form of cell death that also has neuroprotective effects. Cell Counting Kit assay, monodansylcadaverine staining, lfow cytometry, western blotting, and real-time PCR were used to determine the effects of exogenous adenosine triphosphate treatment at different concentrations (2, 4, 6, 8, 10 mmol/L) over time (1, 2, 3, and 6 hours) on the apoptosis and autophagy of SH-SY5Y cells. High concentrations of extracellular adenosine triphosphate induced autophagy and apoptosis of SH-SY5Y cells. The enhanced autophagy ifrst appeared, and peaked at 1 hour after treatment with adenosine triphosphate. Cell apoptosis peaked at 3 hours, and persisted through 6 hours. With prolonged exposure to the adenosine triphosphate treatment, the fraction of apoptotic cells increased. These data suggest that the SH-SY5Y neural cells initiated autophagy against apoptosis within an hour of adenosine triphosphate treatment to protect themselves against injury.

Fatigue is a multifactorial process. Depletion of energy sources, including adenosine triphosphate (ATP), phosphocreatine (PCr), plus carbohydrates (CHO) like muscle glycogen and blood glucose can contribute to fatigue.

三磷酸腺苷辅酶胰岛素静脉滴注诱发冠脉痉挛

患者女,51岁.因阵发性胸闷、心悸半年,加重半个月,于2005年5月10日入院.既往体健,无高血压、糖尿病史、药物过敏史,无家族遗传病史.体格检查:T 36.2℃,P 76次/min,R 20次/min,BP 110/80mmHg(1mm Hg=0.133kPa),HR 76次/min,律不齐,偶可闻及早搏(活动后可闻及早搏2～3次/min),末闻及杂音.辅助检查:心电图示:ST-T轻度改变(下壁、高侧壁),提示偶发室性早搏.动态24 h心电图示:窦性心律,室性早搏共782次,轻度ST-T改变.实验室检查:血常规、肝肾功能、血糖、钾离子、心肌酶谱各项均正常.

线粒体ATP敏感性钾通道激活延缓大鼠心肌缺血引起的细胞间电脱耦联

AIM: To test the hypothesis that cellular uncoupling induced by myocardial ischemia is mediated by activation of mitochondrial ATP-sensitive potassium channels (mitoKATP). METHODS: Rat hearts were perfused on a Langendorff apparatus and subjected to 40-min ischemia followed by 30-min reperfusion (I/R). Changes in cellular coupling were monitored by measuring whole-tissue resistance. RESULTS: (1) In hearts subjected to I/R, the onset of uncoupling started at (13.3±1.0) min of ischemia; (2) Ischemic preconditioning (IPC) delayed the onset of uncoupling until (22.7± 1.3) min. Blocking mitoKATP channels with 5-hydroxydecanoate (5-HD) before the IPC abolished the uncoupling delay [(12.6+1.6) min]; (3) Calcium preconditioning (CPC) had the same effect as IPC. And this effect was reversed by blocking the mitoKATP channel again. In the CPC group the onset of uncoupling occurred after (20.6±1.3) min, and this was canceled by 5-HD [(13.6±0.8) min]; (4) In hearts pretreated with the specific mitoKATP channel opener diazoxide before sustained ischemia, the onset was delayed to (18.4+ 1.4) min; (5) 5-HD canceled the protective effects of diazoxide (12.6±1.0) min; and both the L-type Ca2+ channel inhibitor verapamil and the free radical scavenger N-(2-mercaptopropionyl)glycine, reduced the extended onset time induced by diazoxide [to (13.3± 1.8) min and (13.4±2.1) min, respectively]. CONCLUSION: IPC and CPC delay the onset of cellular uncoupling induced by acute ischemia in rat heart, and the underlying mechanism involves activation of the mitoKATP channels.

Objective:To study the expression of aminopeptidase N (CD13) in renal carcinoma and the effect of CD13 expression vector transfection on biological behavior of cancer cells.Methods:Renal carcinoma tissue and normal kidney tissue were collected and APN (CD13) contents in tissue were detected; renal carcinoma cell lines kevt-3 were cultured, 0 μg/mL, 10 μg/mL, 20 μg/mL, 40 μg/mL and 80 μg/mL of CD13 expression vector were transfected, and then migration ability, ATP generation capacity, and mRNA contents of migration and angiogenesis genes in cells were detected.Results:mRNA contents of APN in renal carcinoma tissue were higher than those in normal kidney tissue; the higher the clinical stage and pathological grade were, the higher the mRNA contents of APN in renal carcinoma tissue were; mRNA levels of APN in renal carcinoma tissue with lymph node metastasis were higher than those without lymph node metastasis;CD13 expression vector transfection could dose-dependently increase kevt-3 cell migration rate, ATP generation amount as well as mRNA contents of VEGF, HIF-1α, MMP9 and MMP10.Conclusion: Expression of aminopeptidase N (CD13) in renal carcinoma tissue abnormally increases; overexpression of CD13 can promote renal carcinoma cell migration and increase ATP generation as well as VEGF, HIF-1, MMP9 and MMP10 expression.