scholarly journals Protective effects of autophagy and NFE2L2 on reactive oxygen species-induced pyroptosis of human nucleus pulposus cells

Aging ◽  
2020 ◽  
Vol 12 (8) ◽  
pp. 7534-7548 ◽  
Author(s):  
Zhibiao Bai ◽  
Wei Liu ◽  
Danshuang He ◽  
Yiyang Wang ◽  
Weiwei Yi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nucleus Pulposus ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Protective Effects ◽  
Nucleus Pulposus Cells

scholarly journals Reactive Oxygen Species Regulate Endoplasmic Reticulum Stress and ER-Mitochondrial Ca2+ Crosstalk to Promote Programmed Necrosis of Rat Nucleus Pulposus Cells under Compression

2021 ◽  
Vol 2021 ◽  
pp. 1-20
Author(s):  
Hui Lin ◽  
Yizhong Peng ◽  
Jinye Li ◽  
Zhe Wang ◽  
Sheng Chen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endoplasmic Reticulum ◽  
Nucleus Pulposus ◽  
Molecular Mechanisms ◽  
Therapeutic Targets ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Nucleus Pulposus Cells ◽  
Programmed Necrosis ◽  
Selective Channel

Programmed necrosis of nucleus pulposus (NP) cells caused by excessive compression is a crucial factor in the etiopathogenesis of intervertebral disc degeneration (IVDD). The endoplasmic reticulum (ER) and mitochondria are crucial regulators of the cell death signaling pathway, and their involvement in IVDD has been reported. However, the specific role of ER stress (ERS) and ER-mitochondria interaction in compression-induced programmed necrosis of NP cells remains unknown. Our studies revealed that compression enhanced ERS and the association between ER and mitochondria in NP cells. Suppression of ERS via 4-phenylbutyrate (4-PBA) or ER-mitochondrial Ca2+ crosstalk by inhibiting the inositol 1,4,5-trisphosphate receptor, glucose-regulated protein 75, voltage-dependent anion-selective channel 1 complex (IP3R–GRP75–VDAC1 complex) protected NP cells against programmed necrosis related to the poly(ADP-ribose) polymerase (PARP) apoptosis-inducing factor (AIF) pathway. Moreover, excessive reactive oxygen species are critical activators of ERS, leading to mitochondrial Ca2+ accumulation and consequent programmed necrosis. These data indicate that ERS and ER-mitochondrial Ca2+ crosstalk may be potential therapeutic targets for the treatment of IVDD-associated disorders. These findings provide new insights into the molecular mechanisms underlying IVDD and may provide novel therapeutic targets.

Protective effects of Brazilian native fruits against reactive oxygen species

Planta Medica ◽  
2014 ◽  
Vol 80 (10) ◽  
Author(s):  
J Infante ◽  
A Massarioli ◽  
PL Rosalen ◽  
S Alencar
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Protective Effects

Anesthetic Preconditioning Improves Adenosine Triphosphate Synthesis and Reduces Reactive Oxygen Species Formation in Mitochondria after Ischemia by a Redox Dependent Mechanism

2003 ◽  
Vol 98 (5) ◽  
pp. 1155-1163 ◽  
Author(s):  
Enis Novalija ◽  
Leo G. Kevin ◽  
Janis T. Eells ◽  
Michele M. Henry ◽  
David F. Stowe
Keyword(s):  
Reactive Oxygen Species ◽  
Cardiac Function ◽  
Adenosine Triphosphate ◽  
Reactive Oxygen ◽  
Atp Synthesis ◽  
Ros Generation ◽  
Oxygen Species ◽  
Protective Effects ◽  
Anesthetic Preconditioning ◽  
Species Formation

Background Mitochondrial changes that characterize the heart after anesthetic preconditioning (APC) or the mechanisms by which mitochondrial triggering factors lead to protection are unknown. This study hypothesized that generation of reactive oxygen species (ROS) during APC is required to initiate the mitochondrial protective effects, and that APC leads to improved mitochondrial electron transport chain function and cardiac function during reperfusion. Methods Isolated guinea pig hearts were subject to 30 min ischemia and 120 min reperfusion. Prior to ischemia hearts were either untreated (I/R), or treated with sevoflurane (APC), in the presence or absence of the ROS scavenger tiron (TIR), or the superoxide dismutase mimetic MnTBAP (TBAP). Intracellular ROS were measured by spectrofluorometry using the fluorescent probe dihydroethidium (DHE). In another series of experiments, using the same protocol, hearts were reperfused for only 5 min and removed for measurement of adenosine triphosphate (ATP) synthesis by luciferin-luciferase luminometry and ROS generation by dichlorohydro-fluorescein (DCF) fluorescence in isolated mitochondria. Results The APC improved cardiac function and reduced infarction. Tiron or MnTBAP abrogated the protection afforded by APC. Mitochondrial ATP synthesis was decreased by 70 +/- 3% after IR alone, by only 7 +/- 3% after APC, by 69 +/- 2% after APC+TIR, and by 71 +/- 3% after APC + TBAP. Mitochondrial ROS formation (DCF) increased by 48 +/- 3% after IR alone, by 0 +/- 2% after APC, by 43 +/- 4% after APC + TIR, and by 46 +/- 3% after APC + TBAP. ROS generation (DHE) was increased in I/R group at 5 and 120 min reperfusion. This was attenuated by APC but this protective effect was abrogated in APC + TIR and APC + TBAP groups. Conclusions The results indicate that ROS are central both in triggering and mediating APC, and that the mitochondrion is the target for these changes.

Protective effects of myricitrin against osteoporosis via reducing reactive oxygen species and bone-resorbing cytokines

2014 ◽  
Vol 280 (3) ◽  
pp. 550-560 ◽  
Author(s):  
Qiang Huang ◽  
Bo Gao ◽  
Long Wang ◽  
Ya-Qian Hu ◽  
Wei-Guang Lu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Protective Effects
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