Metformin protects PC12 cells and hippocampal neurons from H 2 O 2 ‐induced oxidative damage through activation of AMPK pathway

2019 ◽  
Vol 234 (9) ◽  
pp. 16619-16629 ◽  
Author(s):  
Xia Zhao ◽  
Zhiwen Zeng ◽  
Uma Gaur ◽  
Jiankang Fang ◽  
Tangming Peng ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Pc12 Cells ◽  
Hippocampal Neurons ◽  
Ampk Pathway

Marein protects against methylglyoxal-induced apoptosis by activating the AMPK pathway in PC12 cells

2016 ◽  
Vol 50 (11) ◽  
pp. 1173-1187 ◽  
Author(s):  
Baoping Jiang ◽  
Liang Le ◽  
Haibo Liu ◽  
Lijia Xu ◽  
Chunnian He ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Ampk Pathway ◽  
Induced Apoptosis

Effect of food matrices on the in vitro bioavailability and oxidative damage in PC12 cells of lead

2018 ◽  
Vol 266 ◽  
pp. 397-404 ◽  
Author(s):  
Ji Xia ◽  
Yong Fang ◽  
Yi Shi ◽  
Xinchun Shen ◽  
Jian Wu ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Pc12 Cells ◽  
Effect Of Food ◽  
Food Matrices

Lipophilic ferulic acid derivatives protect PC12 cells against oxidative damage via modulating β-amyloid aggregation and activating Nrf2 enzymes

2020 ◽  
Vol 11 (5) ◽  
pp. 4707-4718 ◽  
Author(s):  
Yu Wu ◽  
Yu-gang Shi ◽  
Xiao-liang Zheng ◽  
Ya-li Dang ◽  
Chen-min Zhu ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Oxidative Damage ◽  
Ferulic Acid ◽  
Pc12 Cells ◽  
Amyloid Beta ◽  
Neuroprotective Effect ◽  
Amyloid Aggregation ◽  
Β Amyloid

Ferulic acid (FA) has been shown to have a neuroprotective effect on Alzheimer's disease induced by amyloid-beta (Aβ) neurotoxicity.

scholarly journals NLRC5 alleviated OGD/R-induced PC12-cell injury by inhibiting activation of the TLR4/MyD88/NF-κB pathway

2020 ◽  
Vol 48 (8) ◽  
pp. 030006052094045
Author(s):  
Zhen Zhang ◽  
Yuhan Sun ◽  
Xin Chen
Keyword(s):  
Cerebral Ischemia ◽  
Oxidative Damage ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Injury ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Apoptosis Rate

Objective To assess the role of NOD-like receptor C5 (NLRC5; a major NLRC family protein that regulates immunity, inflammation and tissue fibrosis), in cerebral ischemia-reperfusion injury, characterized by inflammation and oxidative damage. Methods Blood NLRC5 levels were assessed in neonates with cerebral ischemia and in healthy controls. A stable PC12 cell line was established that overexpressed or knocked down NLRC5. Inflammatory responses, apoptosis rate and oxidative damage in PC12 cells under oxygen-glucose deprivation/reperfusion (OGD/R) conditions were evaluated using enzyme-linked immunosorbent assay (ELISA), terminal deoxynucleotidyl transferase dUTP nick end labelling (TUNEL) and reactive oxygen species (ROS) assay. Results Blood NLRC5 levels were suppressed in neonates with cerebral ischemia. ELISAs showed that NLRC5 suppressed levels of tumour necrosis factor-α, interleukin (IL)-6, IL-1β, ROS and superoxide dismutase in OGD/R-treated PC12 cells. Furthermore, NLRC5 overexpression was associated with reduced apoptosis rate in PC12 cells treated by OGD/R. Overexpression of NLRC5 also inhibited levels of toll-like receptor (TLR)4, myeloid differentiation primary response protein MyD88 (MyD88) and phosphorylated nuclear factor kappa B-transcription factor p65 (NF-κB p-p65) in PC12 cells, and decreased nuclear levels of NF-κB p-p65. Conclusion NLRC5 alleviated inflammatory responses, oxidative damage and apoptosis in PC12 cells under OGD/R conditions by suppressing activation of the TLR4/MyD88/NF-κB pathway.

Gnaq Protects PC12 Cells from Oxidative Damage by Activation of Nrf2 and Inhibition of NF-kB

2020 ◽  
Vol 22 (3) ◽  
pp. 401-410
Author(s):  
Xin Sun ◽  
Guo-Ping Li ◽  
Pu Huang ◽  
Lu-Gang Wei ◽  
Jia-Zhi Guo ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Pc12 Cells

scholarly journals Akt attenuates apoptotic death through phosphorylation of H2A under hydrogen peroxide-induced oxidative stress in PC12 cells and hippocampal neurons

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Ji Hye Park ◽  
Chung Kwon Kim ◽  
Sang Bae Lee ◽  
Kyung-Hoon Lee ◽  
Sung-Woo Cho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Pc12 Cells ◽  
Hippocampal Neurons ◽  
Apoptotic Death

scholarly journals Glycine Protects against Hypoxic-Ischemic Brain Injury by Regulating Mitochondria-Mediated Autophagy via the AMPK Pathway

2019 ◽  
Vol 2019 ◽  
pp. 1-29 ◽  
Author(s):  
Chen-chen Cai ◽  
Jiang-hu Zhu ◽  
Li-xia Ye ◽  
Yuan-yuan Dai ◽  
Ming-chu Fang ◽  
...  
Keyword(s):  
Pc12 Cells ◽  
Adenosine Monophosphate ◽  
Ischemic Brain Injury ◽  
Hypoxic Stress ◽  
Ischemic Brain ◽  
Ampk Pathway ◽  
Amp Activated Protein Kinase ◽  
Ischemic Encephalopathy

Hypoxic-ischemic encephalopathy (HIE) is detrimental to newborns and is associated with high mortality and poor prognosis. Thus, the primary aim of the present study was to determine whether glycine could (1) attenuate HIE injury in rats and hypoxic stress in PC12 cells and (2) downregulate mitochondria-mediated autophagy dependent on the adenosine monophosphate- (AMP-) activated protein kinase (AMPK) pathway. Experiments conducted using an in vivo HIE animal model and in vitro hypoxic stress to PC12 cells revealed that intense autophagy associated with mitochondrial function occurred during in vivo HIE injury and in vitro hypoxic stress. However, glycine treatment effectively attenuated mitochondria-mediated autophagy. Additionally, after identifying alterations in proteins within the AMPK pathway in rats and PC12 cells following glycine treatment, cyclosporin A (CsA) and 5-aminoimidazole-4-carboxamide-1-b-4-ribofuranoside (AICAR) were administered in these models and indicated that glycine protected against HIE and CoCl2 injury by downregulating mitochondria-mediated autophagy that was dependent on the AMPK pathway. Overall, glycine attenuated hypoxic-ischemic injury in neurons via reductions in mitochondria-mediated autophagy through the AMPK pathway both in vitro and in vivo.

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