|1.||Chung, Jing-Gung: 22 articles (07/2014 - 11/2004)|
|2.||Wang, Wei: 18 articles (12/2014 - 11/2002)|
|3.||Zhang, John H: 17 articles (01/2016 - 07/2003)|
|4.||Yang, Bin: 14 articles (01/2015 - 10/2002)|
|5.||Zhang, Jie: 13 articles (12/2015 - 09/2005)|
|6.||Gao, Feng: 13 articles (08/2015 - 09/2003)|
|7.||Li, Yan: 13 articles (07/2015 - 10/2003)|
|8.||Li, Wei: 13 articles (10/2014 - 06/2002)|
|9.||Yang, Jai-Sing: 13 articles (07/2014 - 10/2006)|
|10.||Choi, Yung Hyun: 13 articles (06/2010 - 11/2003)|
01/01/2014 - "Furthermore, we report that more potent induction of cell cycle arrest and apoptotic cell death, along with promoted activation of Caspase 3 and autophagy might mechanistically underlie the improved anti-tumor efficacy of HMSNs-BTZ. "
01/01/2012 - "Immunohistochemical analysis of the tumor tissues from animals treated with WFA/Dox combination showed a significant reduction in cell proliferation and formation of microvessels accompanied by increased in LC3B level, cleaved caspase 3, and DNA damage. "
08/01/2003 - "These results indicate that therapeutic attempts to induce caspase-3 in malignant cells may prove useful in the treatment of bcl-x(L)-expressing tumors."
01/01/2000 - "These findings suggest that caspase-3 may mediate apoptosis induced by CDDP, and its induction could represent a novel approach to the effective treatment of malignant tumors."
02/01/2005 - "The sequential treatment of mice with chemotherapeutic drugs followed by TRAIL induced caspase-3 activity, and apoptosis, inhibited angiogenesis, completely eradicated the established tumors, and enhanced survival of mice. "
01/01/2011 - "In ischemia group, the protein of caspase-3 was over-expressed at 6 hours and relieved at 24 hours and 72 hours, while with drug treatment, the expression of protein of caspase-3 was decreased at each time point. "
01/01/2014 - "In this study, we first tested the neuroprotective effect of MVIIC on slices of spinal cord subjected to ischemia evaluating cell death and caspase-3 activation. "
10/01/2004 - "This study aimed at investigating the correlation between the change of ischemic neuronal injury and Caspase-3 post-ischemia in human hippocampus. "
11/27/2001 - "In the present study, we examined if cerebral ischemic tolerance induced by sublethal ischemia is associated with an attenuation of caspase-3 activation in a mouse forebrain ischemia model. "
11/01/2001 - "This study was designed to demonstrate that intermittent ischemia could improve postischemic survival rates by a decrease of JNK(1)/SAPK(1) and caspase 3 activation, which were involved in the apoptosis process. "
04/01/2015 - "We found that (1) TNFR:Fc gene improved cardiac function (EF, LVESP, LVEDP and dp/dt max) post I/R-induced AMI; (2) TNFR:Fc gene inhibited I/R-induced apoptosis and attenuated the level of TNF-α in serum and cardiac tissue; (3) TNFR:Fc gene prevented apoptosis in hypoxia/reoxygenation-induced H9c2 rat cardiomyocytes associated with inhibition of caspase-3 activation and normalization of ratio of the Bcl-2/Bax. "
05/01/2014 - "This study aims at assessing different procedures using an extracorporeal perfusion and oxygenation system to investigate the expression of hypoxia inducible factor (HIF)-1-α as marker for hypoxia and of the pro-apoptotic protein Caspase-3 in skeletal muscle to elucidate potential improvements in tissue conservation. "
07/01/2008 - "The present study tested the hypothesis that mechanism of DNA fragmentation during hypoxia in the cerebral cortex of newborn piglets is mediated by caspase-9-dependent caspase-3 activation. "
03/01/2008 - "Overall results of the present study indicate that hypoxia induces luteal cell apoptosis by enhancing the expression of proapoptotic protein, BNIP3, and by activating caspase-3, and that the induction of apoptosis by hypoxia is partially caused by a decrease in P4 production. "
10/01/2005 - "While fundamental differences between hypoxia/ischaemia in culture and in vivo likely explain the different temporal profiles of Nix, Bax, and caspase-3 activation observed, these studies show that like Bax, mitochondrial accumulation is a common event during Nix activation. "
08/01/2014 - "In addition, sites with inflammation and PD ≥5 mm had significantly greater odds of exhibiting Fas, sFasL, and caspase-3 expression compared with sites without inflammation and PD <5 mm (P <0.05). "
03/01/2014 - "Administration of E(2) resulted in a significant reduction of all serum and liver tissue parameters of inflammation (e.g.decreased iNOS; 193 ± 28 mg/ml and COX-2; 27.6 ± 3.91 U/ml) and decreased apoptosis (Caspase 3; 1.18 ± 0.21 ng/ml). "
01/01/2013 - "Taken together, it has been demonstrated, for the first time, that HBSP effectively improved renal function and tissue damage caused by IR and/or CsA, which might be through reducing caspase-3 activation and synthesis, apoptosis, and inflammation. "
11/20/2015 - "Consistent with the role of GPX4 as a ferroptosis inhibitor, spinal motor neuron degeneration induced by Gpx4 ablation exhibited features of ferroptosis, including no caspase-3 activation, no TUNEL staining, activation of ERKs, and elevated spinal inflammation. "
11/15/2015 - "Further, RUV reduced testicular inflammation and cell death by decreasing the expressions of iNOS, NF-κB and caspase-3. "
08/01/2015 - "It has previously been demonstrated that phosphatidylinositol-3-kinase (PI3K)/Akt and cleaved caspase-3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. "
01/01/2015 - "Xuesaitong can effectively alleviate intestinal barrier dysfunction caused by ischemia-reperfusion injury by reducing TNF-α, up-regulating Bcl-2 and down-regulating caspase-3 expression, in addition to increasing peristalsis."
02/01/2013 - "In SAP, waterfall-style release of inflammatory factors such as TNF-α led to ischemia-reperfusion injury of gut mucosa which resulted in serious oxidative stress and activation of caspase-3 pathway and severe apoptosis of gut mucosa. "
12/01/2012 - "While the volume of tissue at risk by diffusion-weighted magnetic resonance imaging during MCAO was similar in neonatal CD36ko and WT mice, by 24 hours after reperfusion, injury was more severe in CD36ko and was associated with increased caspase-3 cleavage and reduced engulfment of neurons expressing cleaved caspase-3 by activated microglia. "
01/01/2012 - "When subjected to ischemia/reperfusion injury, miR-1 overexpression exacerbated cardiac injury, manifested by increased LDH, CK levels, caspase-3 expression, apoptosis and cardiac infarct area. "
|1.||Cytochromes c (Cytochrome c)
|2.||Messenger RNA (mRNA)
|3.||Proteins (Proteins, Gene)
|5.||Caspase 8 (Caspase-8)
|6.||Small Interfering RNA (siRNA)
|8.||DNA (Deoxyribonucleic Acid)
|10.||Vascular Endothelial Growth Factor A (Vascular Endothelial Growth Factor)
|1.||Heterologous Transplantation (Xenotransplantation)
|2.||Drug Therapy (Chemotherapy)