scholarly journals Protective Effect of Ferulic Acid against Hydrogen Peroxide Induced Apoptosis in PC12 Cells

Molecules ◽  
2020 ◽  
Vol 26 (1) ◽  
pp. 90
Author(s):  
Hironao Nakayama ◽  
Masako Nakahara ◽  
Erina Matsugi ◽  
Midori Soda ◽  
Tomoka Hattori ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Ferulic Acid ◽  
Pc12 Cells ◽  
Pc12 Cell ◽  
Cell Injury ◽  
Biological Effects ◽  
Extracellular Signal ◽  
Pheochromocytoma Pc12 ◽  
Induced Apoptosis ◽  
Related Proteins

Ferulic Acid (FA) is a highly abundant phenolic phytochemical which is present in plant tissues. FA has biological effects on physiological and pathological processes due to its anti-apoptotic and anti-oxidative properties, however, the detailed mechanism(s) of function is poorly understood. We have identified FA as a molecule that inhibits apoptosis induced by hydrogen peroxide (H2O2) or actinomycin D (ActD) in rat pheochromocytoma, PC12 cell. We also found that FA reduces H2O2-induced reactive oxygen species (ROS) production in PC12 cell, thereby acting as an anti-oxidant. Then, we analyzed FA-mediated signaling responses in rat pheochromocytoma, PC12 cells using antibody arrays for phosphokinase and apoptosis related proteins. This FA signaling pathway in PC12 cells includes inactivation of pro-apoptotic proteins, SMAC/Diablo and Bad. In addition, FA attenuates the cell injury by H2O2 through the inhibition of phosphorylation of the extracellular signal-regulated kinase (ERK). Importantly, we find that FA restores expression levels of brain-derived neurotrophic factor (BDNF), a key neuroprotective effector, in H2O2-treated PC12 cells. As a possible mechanism, FA increases BDNF by regulating microRNA-10b expression following H2O2 stimulation. Taken together, FA has broad biological effects as a neuroprotective modulator to regulate the expression of phosphokinases, apoptosis-related proteins and microRNAs against oxidative stress in PC12 cells.

scholarly journals New Cyclic Diarylheptanoids from Platycarya strobilacea

Molecules ◽  
2020 ◽  
Vol 25 (24) ◽  
pp. 6034
Author(s):  
Wen-bing Ding ◽  
Rui-yuan Zhao ◽  
Guan-hua Li ◽  
Bing-lei Liu ◽  
Hua-liang He ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Pc12 Cells ◽  
Stem Bark ◽  
No Production ◽  
Electronic Circular Dichroism ◽  
Pheochromocytoma Pc12 ◽  
Pheochromocytoma Pc12 Cells ◽  
Induced Apoptosis ◽  
Circular Dichroïsm

Five new cyclic diarylheptanoids (platycary A–E, compounds 1–5) and three previously identified analogues (i.e., phttyearynol (compound 6), myricatomentogenin (compound 7), and juglanin D (compound 8)) were isolated from the stem bark of Platycarya strobilacea. The structures of these compounds were determined using NMR, HRESIMS, and electronic circular dichroism (ECD) data. The cytotoxicity of compounds 1–5 and their ability to inhibit nitric oxide (NO) production, as well as protect against the corticosterone-induced apoptosis of Pheochromocytoma (PC12) cells, were evaluated in vitro using the appropriate bioassays. Compounds 1 and 2 significantly inhibited the corticosterone-induced apoptosis of PC12 cells at a concentration of 20 μΜ.

Local Anesthetics Inhibit Muscarinic Receptor-mediated Activation of Extracellular Signal-regulated Kinases in Rat Pheochromocytoma PC12 Cells 

1999 ◽  
Vol 91 (4) ◽  
pp. 1014-1014 ◽  
Author(s):  
Zhiming Tan ◽  
Shuji Dohi ◽  
Kenji Ohguchi ◽  
Shigeru Nakashima ◽  
Yoshinori Nozawa
Keyword(s):  
Tyrosine Phosphorylation ◽  
Pc12 Cells ◽  
Acetylcholine Receptor ◽  
Local Anesthetics ◽  
Muscarinic Acetylcholine Receptor ◽  
Erk Activation ◽  
Muscarinic Acetylcholine ◽  
M3 Muscarinic Acetylcholine Receptor ◽  
Extracellular Signal ◽  
Pheochromocytoma Pc12

Background Because protein phosphorylation is a key mechanism for controlling cellular functions and extracellular signal-regulated kinase (ERK) plays a role in cellular signal transduction, the authors wanted to determine whether local anesthetics interfere with biochemical signaling molecules. Methods Protein tyrosine phosphorylation and ERK activation induced by carbachol, an agonist for muscarinic acetylcholine receptors, were examined in rat pheochromocytoma PC12 cells, a model for investigating signal transduction. Carbachol-induced tyrosine-phosphorylated proteins of 44 and 42 kd were determined by Western blot analysis and identified as activated ERK1 and ERK2 using anti-ERK antibody. The ERK activation was blocked by preincubation with atropine or an M3 muscarinic acetylcholine receptor antagonist 4-diphenyacetooxy-1, 1-dimethylpiperidinium, indicating that is was mediated by M3 muscarinic acetylcholine receptor activation. Then, in the presence of local anesthetic, the carbachol-induced tyrosine phosphorylation and ERK activation were evaluated. The effects of three Na+ current-modifying reagents on carbachol-induced ERK activation were also evaluated. Results Procaine (10(-4) to 10(-3) M) inhibited carbachol-induced tyrosine phosphorylation and ERK activation in a concentration-dependent manner. Although tetracaine, lidocaine, and bupivacaine similarly suppressed carbachol-induced tyrosine phosphorylation and ERK activation, neither tetrodotoxin, veratridine, nor ouabain affected the carbachol-induced ERKs activation. Both ERKs were also activated by 4beta-phorbol 12-myristate 13-acetate, an activator of protein kinase C, and fluoroaluminate (AlF4-), respectively, but procaine did not affect ERK activation induced by these two substances. The inhibition of carbachol-induced ERK activation by procaine was not modified by a phosphatase inhibitor, calyculin A. Conclusions The current results indicate that local anesthetics inhibit the activity of the signal-transducing molecule(s) leading to M3 muscarinic acetylcholine receptor-mediated ERK activation in PC12 cells. Such action is unlikely to be a result of the drug's action on Na+ channels or on the electrochemical gradients of the neuronal cell membrane.

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.

Chloride channels involve in hydrogen peroxide-induced apoptosis of PC12 cells

2009 ◽  
Vol 387 (4) ◽  
pp. 666-670 ◽  
Author(s):  
Wanhong Zuo ◽  
Linyan Zhu ◽  
Zhiquan Bai ◽  
Haifeng Zhang ◽  
Jianwen Mao ◽  
...  
Keyword(s):  
Hydrogen Peroxide ◽  
Pc12 Cells ◽  
Chloride Channels ◽  
Induced Apoptosis
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