scholarly journals Antioxidative stress effects of Humulus japonicus extracts on neuronal PC12 cells

Author(s):  
Feng WANG ◽  
Jae Young SHIN ◽  
Byoung Ok CHO ◽  
Suping HAO ◽  
Ji Hyeon PARK ◽  
...  
2008 ◽  
Vol 1 (1) ◽  
pp. 54-62 ◽  
Author(s):  
Vicky Lahaie-Collins ◽  
Julie Bournival ◽  
Marilyn Plouffe ◽  
Julie Carange ◽  
Maria-Grazia Martinoli

Oxidative stress is regarded as a mediator of nerve cell death in several neurodegenerative disorders, such as Parkinson's disease. Sesamin, a lignan mainly found in sesame oil, is currently under study for its anti-oxidative and possible neuroprotective properties. We used 1-methyl-4-phenyl-pyridine (MPP+) ion, the active metabolite of the potent parkinsonism-causing toxin 1-methyl-4-phenyl-1,2,5,6-tetrahydropyridine, to produce oxidative stress and neurodegeneration in neuronal PC12 cells, which express dopamine, as well as neurofilaments. Our results show that picomolar doses of sesamin protected neuronal PC12 cells from MPP+-induced cellular death, as revealed by colorimetric measurements and production of reactive oxygen species. We also demonstrated that sesamin acted by rescuing tyrosine hydroxylase levels from MPP+-induced depletion. Sesamin, however, did not modulate dopamine transporter levels, and estrogen receptor-alpha and -beta protein expression. By examining several parameters of cell distress, we found that sesamin also elicited a strong increase in superoxide dismutase activity as well as protein expression and decreased catalase activity and the MPP+stimulated inducible nitric oxide synthase protein expression, in neuronal PC12 cells. Finally, sesamin possessed significant anti-inflammatory properties, as disclosed by its potential to reduce MPP+-induced interleukin-6 mRNA levels in microglia. From these studies, we determined the importance of the lignan sesamin as a neuroprotective molecule and its possible role in complementary and/or preventive therapies of neurodegenerative diseases.


2006 ◽  
Vol 99 (4) ◽  
pp. 1282-1298 ◽  
Author(s):  
M. C. Morsink ◽  
M. Joëls ◽  
R. A. Sarabdjitsingh ◽  
O. C. Meijer ◽  
E. R. De Kloet ◽  
...  

2003 ◽  
Vol 67 (6) ◽  
pp. 1312-1318 ◽  
Author(s):  
Hideo SATSU ◽  
Tatsuya YOKOYAMA ◽  
Nobumasa OGAWA ◽  
Yoko FUJIWARA-HATANO ◽  
Makoto SHIMIZU

1992 ◽  
Vol 119 (6) ◽  
pp. 1669-1680 ◽  
Author(s):  
P W Mesner ◽  
T R Winters ◽  
S H Green

Previous studies have shown that in neuronal cells the developmental phenomenon of programmed cell death is an active process, requiring synthesis of both RNA and protein. This presumably reflects a requirement for novel gene products to effect cell death. It is shown here that the death of nerve growth factor-deprived neuronal PC12 cells occurs at the same rate as that of rat sympathetic neurons and, like rat sympathetic neurons, involves new transcription and translation. In nerve growth factor-deprived neuronal PC12 cells, a decline in metabolic activity, assessed by uptake of [3H]2-deoxyglucose, precedes the decline in cell number, assessed by counts of trypan blue-excluding cells. Both declines are prevented by actinomycin D and anisomycin. In contrast, the death of nonneuronal (chromaffin-like) PC12 cells is not inhibited by transcription or translation inhibitors and thus does not require new protein synthesis. DNA fragmentation by internucleosomal cleavage does not appear to be a consistent or significant aspect of cell death in sympathetic neurons, neuronal PC12 cells, or nonneuronal PC12 cells, notwithstanding that the putative nuclease inhibitor aurintricarboxylic acid protects sympathetic neurons, as well as neuronal and nonneuronal PC12 cells, from death induced by trophic factor removal. Both phenotypic classes of PC12 cells respond to aurintricarboxylic acid with similar dose-response characteristics. Our results indicate that programmed cell death in neuronal PC12 cells, but not in nonneuronal PC12 cells, resembles programmed cell death in sympathetic neurons in significant mechanistic aspects: time course, role of new protein synthesis, and lack of a significant degree of DNA fragmentation.


2020 ◽  
Vol 2020 ◽  
pp. 1-15
Author(s):  
Dejene Disasa ◽  
Lihong Cheng ◽  
Majid Manzoor ◽  
Qian Liu ◽  
Ying Wang ◽  
...  

In the present study, the replicative lifespan assay of yeast was used to guide the isolation of antiaging substance from Gentiana rigescens Franch, a traditional Chinese medicine. A compound with antiaging effect was isolated, and the chemical structure of this molecule as amarogentin was identified by spectral analysis and compared with the reported data. It significantly extended the replicative lifespan of K6001 yeast at doses of 1, 3, and 10 μM. Furthermore, amarogentin improved the survival rate of yeast under oxidative stress by increasing the activities of catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx), and these enzymes’ gene expression. In addition, this compound did not extend the replicative lifespan of sod1, sod2, uth1, and skn7 mutants with K6001 background. These results suggested that amarogentin exhibited antiaging effect on yeast via increase of SOD2, CAT, GPx gene expression, enzyme activity, and antioxidative stress. Moreover, we evaluated antioxidant activity of this natural products using PC12 cell system, a useful model for studying the nervous system at the cellular level. Amarogentin significantly improved the survival rate of PC12 cells under H2O2-induced oxidative stress and increased the activities of SOD and SOD2, and gene expression of SOD2, CAT, GPx, Nrf2, and Bcl-x1. Meanwhile, the levels of reactive oxygen species (ROS) and malondialdehyde (MDA) of PC12 cells were significantly reduced after treatment of the amarogentin. These results indicated that antioxidative stress play an important role for antiaging and neuroprotection of amarogentin. Interestingly, amarogentin exhibited neuritogenic activity in PC12 cells. Therefore, the natural products, amarogentin from G. rigescens with antioxidant activity could be a good candidate molecule to develop drug for treating neurodegenerative diseases.


2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Adriana E. Bulboacă ◽  
Sorana D. Bolboacă ◽  
Ioana C. Stănescu ◽  
Carmen A. Sfrângeu ◽  
Angelo C. Bulboacă

Objective. Our study aimed to investigate the analgesic and antioxidative stress effects of Curcumin (CC) in experimental migraine induced by Nitroglycerin (NTG) on rats, compared with Indomethacin (ID) and Propranolol (PP) treatments. Material and Methods. Five groups of 10 rats treated i.p. were investigated: control group (healthy rats) injected with saline solution (0.9%), NTG-control group injected with NTG (1 mg/100 gbw, bw = body weight), and three groups with pretreatment applied 30 min previous to the formalin test (NTG + CC group: Curcumin (10 mg/100 gbw), NTG + PP group: Propranolol (100 μg/100 gbw), and NTG + ID group: Indomethacin (0.5 mg/100 gbw)). Formalin test was performed and number of flinches and shakes were counted. Several oxidative stress parameters were also assessed. Results. The smallest values of malondialdehyde (MDA), nitric oxide (NOx), and total oxidative status (TOS) were observed on NTG + CC with significant differences as compared with the control group (p<0.0001). The group pretreated with Curcumin proved significantly smaller number of flinches and shakes compared with both NTG + PP and NTG + ID. Conclusion. Our study demonstrates a superior activity of Curcumin not only versus control, but also versus Propranolol and Indomethacin.


2007 ◽  
Vol 85 (12) ◽  
pp. 2702-2713 ◽  
Author(s):  
Graziella Cappelletti ◽  
Mariarita Galbiati ◽  
Cristina Ronchi ◽  
Maria Grazia Maggioni ◽  
Elisa Onesto ◽  
...  

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