scholarly journals Apigenin Combined With Gefitinib Blocks Autophagy Flux and Induces Apoptotic Cell Death Through Inhibition of HIF-1α, c-Myc, p-EGFR, and Glucose Metabolism in EGFR L858R+T790M-Mutated H1975 Cells

2019 ◽  
Vol 10 ◽  
Author(s):  
ZiSheng Chen ◽  
Dongbo Tian ◽  
Xiaowen Liao ◽  
Yifei Zhang ◽  
Jinghua Xiao ◽  
...  
Keyword(s):  
Cell Death ◽  
Glucose Metabolism ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Autophagy Flux

scholarly journals Autophagy Promotes Porcine Parvovirus Replication and Induces Non-Apoptotic Cell Death in Porcine Placental Trophoblasts

Viruses ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 15
Author(s):  
Xiujuan Zhang ◽  
Yingli Xiong ◽  
Jie Zhang ◽  
Ting Shao ◽  
Songbiao Chen ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Porcine Parvovirus ◽  
Caspase Inhibitor ◽  
Autophagy Flux ◽  
Autophagy Induction ◽  
Cellular Apoptosis ◽  
Infected Cells ◽  
Later Phase

Autophagy plays important roles in the infection and pathogenesis of many viruses, yet the regulatory roles of autophagy in the process of porcine parvovirus (PPV) infection remain unclear. Herein, we show that PPV infection induces autophagy in porcine placental trophoblasts (PTCs). Induction of autophagy by rapamycin (RAPA) inhibited the occurrence of apoptotic cell death, yet promoted viral replication in PPV-infected cells; inhibition of autophagy by 3-MA or ATG5 knockdown increased cellular apoptosis and reduced PPV replication. Interestingly, we found that in the presence of caspase-inhibitor zVAD-fmk, PPV induces non-apoptotic cell death that was characterized by lysosomal damage and associated with autophagy. Induction of complete autophagy flux by RAPA markedly promoted PPV replication compared with incomplete autophagy induced by RAPA plus bafilomycin (RAPA/BAF) in the early phase of PPV infection (24 h.p.i.). Meanwhile, induction of complete autophagy with RAPA increased lysosomal damage and non-apoptotic cell death in the later phase of PPV infection. Therefore, our data suggest that autophagy can enhance PPV replication and promote the occurrence of lysosomal-damage-associated non-apoptotic cell death in PPV-infected porcine placental trophoblasts.

scholarly journals Neuroprotective Effects of Pharmacological Hypothermia on Glucose Metabolism in Ischemic Rats

2021 ◽  
Author(s):  
Longfei Guan ◽  
Hangil Lee ◽  
Xiaokun Geng ◽  
Fengwu Li ◽  
Jiamei Shen ◽  
...  
Keyword(s):  
Cell Death ◽  
Glucose Metabolism ◽  
Apoptotic Cell ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Apoptotic Cell Death ◽  
Neurological Deficits ◽  
Neuroprotective Effects ◽  
Glut 1 ◽  
Atp Levels ◽  
Neuroprotective Strategy

Abstract Stroke is a leading threat to human life. Metabolic dysfunction of glucose may play a key role in stroke pathophysiology. Pharmacological hypothermia (PH) is a potential neuroprotective strategy for stroke in which the temperature can be decreased safely. The present study determined whether neuroprotective PH with chlorpromazine and promethazine (C+P) plus dihydrocapsaicin (DHC) improved glucose metabolism in acute ischemic stroke. A total of 208 adult male Sprague-Dawley rats were randomly divided into the following groups: sham, stroke, and stroke with various treatments including C+P, DHC, C+P+DHC, phloretin (glucose transporter (GLUT)-1 inhibitor), cytochalasin B (GLUT-3 inhibitor), TZD (thiazolidinedione, phosphoenolpyruvate carboxykinase (PCK) inhibitor) and apocynin (nicotinamide adenine dinucleotide phosphate oxidase (NOX) inhibitor). Stroke was induced by middle cerebral artery occlusion (MCAO) for 2 h followed by 6 or 24 h of reperfusion. Rectal temperature was monitored before, during, and after PH. Infarct volume and neurological deficits were measured to assess the neuroprotective effects. Reactive oxygen species (ROS), NOX activity, lactate, apoptotic cell death, glucose, and ATP levels were measured. Protein expressions of GLUT-1, GLUT-3, phosphofructokinase (PFK), lactate dehydrogenase (LDH), PCK1, PCK2, and NOX subunit gp91 were measured with Western blotting. PH with combination of C+P and DHC induced a faster, longer, and deeper hypothermia as compared to each alone. PH significantly improved every measured outcome as compared to stroke and monotherapy. PH reduced brain infarction, neurological deficits, protein levels of glycolytic enzymes (GLUT-1, GLUT-3, PFK and LDH), gluconeogenic enzymes (PCK1 and PCK2), NOX activity and its subunit gp91, ROS, apoptotic cell death, glucose, and lactate, while raising ATP levels. In conclusion, stroke impaired glucose metabolism by enhancing hyperglycolysis and gluconeogenesis, which led to ischemic injury, all of which were reversed by PH induced by a combination of C+P and DHC.

scholarly journals Macrolides sensitize EGFR-TKI-induced non-apoptotic cell death via blocking autophagy flux in pancreatic cancer cell lines

2015 ◽  
Vol 48 (1) ◽  
pp. 45-54 ◽  
Author(s):  
SHUNTARO MUKAI ◽  
SHOTA MORIYA ◽  
MASAKI HIRAMOTO ◽  
HIROMI KAZAMA ◽  
HIROKO KOKUBA ◽  
...  
Keyword(s):  
Pancreatic Cancer ◽  
Cell Death ◽  
Cell Lines ◽  
Cancer Cell ◽  
Pancreatic Cancer Cell ◽  
Apoptotic Cell ◽  
Cancer Cell Lines ◽  
Apoptotic Cell Death ◽  
Autophagy Flux ◽  
Egfr Tki

KIOM-79 prevents apoptotic cell death and AGEs accumulation in the retina of diabetic db/db mice

Planta Medica ◽  
2007 ◽  
Vol 73 (09) ◽  
Author(s):  
YS Kim ◽  
EJ Sohn ◽  
HY Lee ◽  
CS Kim ◽  
YM Lee ◽  
...  
Keyword(s):  
Cell Death ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death

Apoptotic cell death triggered by nitric oxide in pancreatic beta-cells

Diabetes ◽  
1995 ◽  
Vol 44 (7) ◽  
pp. 733-738 ◽  
Author(s):  
H. Kaneto ◽  
J. Fujii ◽  
H. G. Seo ◽  
K. Suzuki ◽  
T. Matsuoka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Beta Cells ◽  
Pancreatic Beta Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death
Sign in / Sign up

Export Citation Format

Share Document