|1.||Gao, Qin: 7 articles (01/2012 - 01/2005)|
|2.||Xia, Qiang: 6 articles (11/2006 - 01/2005)|
|3.||Bruce, Iain C: 4 articles (09/2006 - 01/2005)|
|4.||Faghihi, Mahdieh: 3 articles (08/2015 - 11/2010)|
|5.||Pan, Hong-Yang: 3 articles (11/2006 - 01/2005)|
|6.||Huang, Xuliang: 2 articles (06/2012 - 01/2011)|
|7.||Song, Rui: 2 articles (06/2012 - 01/2011)|
|8.||Bian, Huining: 2 articles (06/2012 - 01/2011)|
|9.||Tosaka, Shinya: 2 articles (01/2012 - 01/2007)|
|10.||Hara, Tetsuya: 2 articles (01/2012 - 01/2007)|
05/26/1976 - "Intracoronary infusion of atractyloside resulted in physiological, biochemical, and ultrastructural changes similar to those seen with ischemia. "
12/07/2005 - "On the other hand, administration of 10 micromol/L NS 1619, an opener of the K(Ca) channel, for 10 min before ischemia, decreased the infarct size and LDH release, and improved contractile functions and CF; these effects were attenuated by atractyloside. "
01/01/2015 - "Sprague Dawley rats (N = 60) were randomly divided into five groups of 12 rats each: control, ischemia/reperfusion (I/R), melatonin treatment (MT), melatonin treatment + atractyloside (MT+ATR), and atractyloside (ATR). "
11/01/2010 - "Administration of atractyloside abolished cardioprotective effects of phenylephrine in both early and late phases and returned infarct size, CK-MB and cardiac function to levels as seen in ischemia/reperfusion group. "
06/13/2006 - "In isolated ventricular myocytes, pretreatment with Pue prevented ischemia-induced cell death and depolarization of the mitochondrial membrane, and atractyloside and 5-hydroxydecanoate attenuated the effects of Pue. "
|2.||Wounds and Injuries (Trauma)
05/01/2013 - "Dex preconditioning markedly improved the myocardial viability and cardiac function (P<0.01), which were reversed by the treatment with both atractyloside (20 μmol/L before ischemia), an opener of mPTP, and 5-hydroxydecanoate (100 μmol/L at the beginning of reperfusion), an inhibitor of mitoKATP, for 20 min. Dex has protective effect against I/R injuries in isolated rat hearts, which may be related to inhibiting the opening of mPTP at the beginning of reperfusion and activating mitoKATP before ischemia."
11/01/2010 - "Seven groups (n = 6) of rats were randomly studied: (I) control: surgical procedure was performed with no ischemia/reperfusion, (II) ischemia/reperfusion: hearts underwent regional ischemia/reperfusion, (III) early phenylephrine: phenylephrine (50 μM) was perfused for 5 min prior to ischemia/reperfusion, (IV) late phenylephrine: rats were treated with phenylephrine (10 mg/kg, i.p) 24 h prior to ischemia/reperfusion, (V) early phenylephrine+atractyloside: hearts were perfused with phenylephrine as in group III and then atractyloside (20 mM) 5 min before reperfusion for 20 min, (VI) late phenylephrine+atractyloside: hearts were treated with phenylephrine as in group IV and then received atractyloside (20 mM), 5 min before reperfusion for 20 min, (VII) atractyloside-IR group: hearts were perfused with atractyloside (20 mM) 5 min before reperfusion for 20 min. Compared with ischemia/reperfusion group, perfusion of phenylephrine in early and late phases decreased myocardial infarct size (% of ischemia zone), reduced creatine kinase-MB (CK-MB) in the coronary effluent, and improved cardiac function. "
11/10/2006 - "Identification of atractyloside by LC-ESI-MS in alleged herbal poisonings."
12/01/2000 - "Simple methods for the detection of atractyloside poisoning are at present restricted to thin-layer chromatography in urine and are useful only in the case of severe poisoning. "
12/01/2000 - "Atractyloside poisoning is an infrequent but often fatal form of herbal poisoning, which occurs worldwide but especially in Africa and the Mediterranean regions. "
10/01/1999 - "This method is rapid and may be used for the definitive diagnosis in cases of poisoning with atractyloside-containing plants."
10/01/1999 - "Cases of poisoning with other plants which contain atractyloside also occur in Europe and the Americas. "
12/01/2000 - "Atractyloside in large amounts gives rise to massive necrosis, but in vitro studies have shown that at lower doses cells progress to apoptosis. "
07/01/1998 - "The toxic and cellular metabolic effects of atractyloside, a diterpenoid glycoside, which causes fatal renal and hepatic necrosis in vivo in animals and humans, have been investigated in tissue slices prepared from male domestic pig kidney and liver. "
|2.||Adenosine Triphosphate (ATP)
|3.||mitochondrial permeability transition pore
|4.||Potassium Channels (Potassium Channel)
|5.||1- Methyl- 4- phenyl- 1,2,3,6- tetrahydropyridine (MPTP)
|6.||mitochondrial K(ATP) channel
|7.||MB Form Creatine Kinase