scholarly journals Inhibition of Production of Reactive Oxygen Species and Gene Expression Profile by Treatment of Ethanol Extract of Moutan Cortex Radicis in Oxidative Stressed PC12 Cells

2005 ◽  
Vol 28 (4) ◽  
pp. 661-666 ◽  
Author(s):  
Samwoong Rho ◽  
Hwan-Suck Chung ◽  
Moonkyu Kang ◽  
Euna Lee ◽  
Chongwoon Cho ◽  
...  
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Pc12 Cells ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Reactive Oxygen ◽  
Ethanol Extract ◽  
Oxygen Species ◽  
Moutan Cortex

scholarly journals Endothelin-2/Vasoactive Intestinal Contractor: Regulation of Expression via Reactive Oxygen Species Induced by CoCl22, and Biological Activities Including Neurite Outgrowth in PC12 Cells

2006 ◽  
Vol 6 ◽  
pp. 176-186 ◽  
Author(s):  
Eiichi Kotake-Nara ◽  
Kaname Saida
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Biological Activities ◽  
Reactive Oxygen ◽  
Neuronal Model ◽  
Oxygen Species ◽  
Regulation Of Expression ◽  
Normal Tissues

This paper reviews the local hormone endothelin-2 (ET-2), or vasoactive intestinal contractor (VIC), a member of the vasoconstrictor ET peptide family, where ET-2 is the human orthologous peptide of the murine VIC. While ET-2/VIC gene expression has been observed in some normal tissues, ET-2 recently has been reported to act as a tumor marker and as a hypoxia-induced autocrine survival factor in tumor cells. A recently published study reported that the hypoxic mimetic agent CoCl2at 200 µM increased expression of the ET-2/VIC gene, decreased expression of the ET-1 gene, and induced intracellular reactive oxygen species (ROS) increase and neurite outgrowth in neuronal model PC12 cells. The ROS was generated by addition of CoCl2to the culture medium, and the CoCl2-induced effects were completely inhibited by the antioxidantN-acetyl cysteine. Furthermore, interleukin-6 (IL-6) gene expression was up-regulated upon the differentiation induced by CoCl2. These results suggest that expression of ET-2/VIC and ET-1 mediated by CoCl2-induced ROS may be associated with neuronal differentiation through the regulation of IL-6 expression. CoCl2acts as a pro-oxidant, as do Fe(II, III) and Cu(II). However, some biological activities have been reported for CoCl2that have not been observed for other metal salts such as FeCl3, CuSO4, and NiCl2. The characteristic actions of CoCl2may be associated with the differentiation of PC12 cells. Further elucidation of the mechanism of neurite outgrowth and regulation of ET-2/VIC expression by CoCl2may lead to the development of treatments for neuronal disorders.

Zn2+-induced ERK activation mediated by reactive oxygen species causes cell death in differentiated PC12 cells

2001 ◽  
Vol 78 (3) ◽  
pp. 600-610 ◽  
Author(s):  
Su Ryeon Seo ◽  
Seon Ah Chong ◽  
Syng-Ill Lee ◽  
Jee Young Sung ◽  
Young Soo Ahn ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Pc12 Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Erk Activation ◽  
Differentiated Pc12 Cells

Protective Effects of Crataegus pinnatifida Extracts and Crataegolic Acid Against Neurotoxicity of Paraquat in PC12 Cells

2021 ◽  
Vol 20 (1) ◽  
pp. 76-83
Author(s):  
Chi-Sen Chang ◽  
Yuh-Chiang Shen ◽  
Chi-Wen Juan ◽  
Chia-Lin Chang ◽  
Po-Kai Lin
Keyword(s):  
Reactive Oxygen Species ◽  
Pc12 Cells ◽  
Cell Apoptosis ◽  
Active Component ◽  
Caspase 3 ◽  
Reactive Oxygen ◽  
B Cell Lymphoma ◽  
Oxygen Species ◽  
Protein Levels ◽  
Crataegus Pinnatifida

The neuroprotective mechanisms of Crataegus pinnatifida extracts and crataegolic acid were studied using paraquat induced cytotoxicity in PC12 cells. C. pinnatifida extracts were prepared using hexane, ethyl acetate, and 95% ethanol. Additionally, crataegolic acid (also known as maslinic acid) was found in C. pinnatifida extracts. Assessment methods included the examinations of cytotoxicity, intracellular reactive oxygen species and calcium changes, activity of caspase-3 and α-synuclein, apoptotic cell death, and the expression levels of the B-cell lymphoma 2 (Bcl-2) and BCL2-associated X (Bax) proteins to investigate the neuroprotective mechanisms of C. pinnatifida extracts and its active component, crataegolic acid. The three extracts and crataegolic acid exhibited potent neuroprotective actions against paraquat induced PC12 cell apoptosis at 5–20µg/mL and 80–100µM concentrations, respectively. The key protective mechanisms included decreasing cell apoptosis, upregulating Bcl-2 protein levels, and downregulating Bax protein levels. The 95% ethanol extract also decreased paraquat induced reactive oxygen species production, calcium overloading, and caspase-3 and α-synuclein activities. The beneficial effects of these extracts could be explained by the active component, crataegolic acid that also inhibited paraquat-induced apoptosis through the suppression of reactive oxygen species generation and the caspase-3 signaling pathway.

scholarly journals Comparison of Efficacies of Different Jakyakgamcho-tang Extracts on H2O2-Induced C2C12 Cell Viability

2020 ◽  
Author(s):  
Young Sook Kim ◽  
Heung Joo Yuk ◽  
Dong-Seon Kim
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Viability ◽  
Muscle Pain ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Ethanol Extract ◽  
Oxygen Species ◽  
Water Extracts ◽  
Ethanol Extracts

Oxidative stress is a major contributor to muscle aging and loss of muscle tissue. Jakyakgamcho-tang has been used in traditional Eastern medicine to treat muscle pain. Here, we compared various solvent-based Jakyakgamcho-tang extracts in terms of their effects against hydrogen peroxide-induced oxidative stress in murine C2C12 skeletal muscle cells. Total phenolic content and total flavonoid content in 30% ethanol extracts of Jakyakgamcho-tang were higher than those of water extracts of Jakyakgamcho-tang. Ethanol extracts of Jakyakgamcho-tang had stronger antioxidant and 2,2-azino-bis-3-ethylbenzothiazoline-6-sulfonic acid and 2,2´-diphenyl-1-picrylhydrazyl-scavenging activity than water extracts of Jakyakgamcho-tang. The ethanol extract of Jakyakgamcho-tang inhibited peroxide-induced cell viability and intracellular reactive oxygen species generation more effectively than the water extract of Jakyakgamcho-tang in a dose-dependent manner. These results suggest that the ethanol extract of Jakyakgamcho-tang is relatively more efficacious at protecting against oxidative stress-induced muscle cell death because it prevents reactive oxygen species generation in C2C12 cells. Moreover, the current study indicated that the effective dose of the ethanol extract of Jakyakgamcho-tang required to alleviate muscle pain might be lower than that required for Jakyakgamcho-tang.

scholarly journals Spatial Regulation of Reactive Oxygen Species via G6PD in Brown Adipocytes Supports Thermogenic Function

2021 ◽  
Author(s):  
Jee Hyung Sohn ◽  
Yul Ji ◽  
Chang-Yun Cho ◽  
Hahn Nahmgoong ◽  
Sangsoo Lim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Redox Potentials ◽  
Brown Adipocytes ◽  
Erk Activation ◽  
Brown Adipose ◽  
Erk Inhibition ◽  
Glucose 6 Phosphate Dehydrogenase

Reactive oxygen species (ROS) are associated with various roles of brown adipocytes. Glucose-6-phosphate dehydrogenase (G6PD) controls cellular redox potentials by producing NADPH. Although G6PD upregulates cellular ROS levels in white adipocytes, the roles of G6PD in brown adipocytes remain elusive. Here, we found that G6PD defect in brown adipocytes impaired thermogenic function through excessive cytosolic ROS accumulation. Upon cold exposure, G6PD-deficient mutant (G6PD<sup>mut</sup>) mice exhibited cold intolerance and downregulated thermogenic gene expression in brown adipose tissue (BAT). In addition, G6PD-deficient brown adipocytes had increased cytosolic ROS levels, leading to ERK activation. In BAT of G6PD<sup>mut</sup> mice, administration of antioxidant restored the thermogenic activity by potentiating thermogenic gene expression and relieving ERK activation. Consistently, body temperature and thermogenic execution were rescued by ERK inhibition in cold-exposed G6PD<sup>mut</sup> mice. Taken together, these data suggest that G6PD in brown adipocytes would protect against cytosolic oxidative stress, leading to cold-induced thermogenesis.

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