scholarly journals Protective Effect of Carnosine Against Zn-Mediated Toxicity in Cortical Neuronal Cells

2007 ◽  
Vol 23 (1) ◽  
pp. 33-38
Author(s):  
Jin-Joo Hue ◽  
Ah-Ram Lee ◽  
Yea-Eun Lee ◽  
Min-Hang Cho ◽  
Ki-Nam Lee ◽  
...  
Keyword(s):  
Protective Effect ◽  
Neuronal Cells

Protective effect of nicotinamide on neuronal cells under oxygen and glucose deprivation and hypoxia/reoxygenation

2004 ◽  
Vol 11 (4) ◽  
pp. 472-481 ◽  
Author(s):  
Chiung-Chyi Shen ◽  
Hsueh-Meei Huang ◽  
Hsiu-Chung Ou ◽  
Huan-Lian Chen ◽  
Wen-Chi Chen ◽  
...  
Keyword(s):  
Protective Effect ◽  
Neuronal Cells ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
Hypoxia Reoxygenation

ChemInform Abstract: Pontemazines A and B, Phenazine Derivatives Containing a Methylamine Linkage from Streptomyces sp. UT1123 and Their Protective Effect to HT-22 Neuronal Cells.

ChemInform ◽  
2016 ◽  
Vol 47 (10) ◽  
pp. no-no
Author(s):  
Jin Wook Cha ◽  
Seung Il Lee ◽  
Min Cheol Kim ◽  
Mya Thida ◽  
Jae Wook Lee ◽  
...  
Keyword(s):  
Protective Effect ◽  
Neuronal Cells ◽  
Streptomyces Sp

The Protective Effect of Picroside II on Isoflurane-Induced Neuronal Injury in Rats via Downregulating miR-195

2021 ◽  
pp. 1-9
Author(s):  
Hui Li ◽  
Weijia Du ◽  
Yawei Yuan ◽  
Jingjing Xue ◽  
Qiang Li ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Protective Effect ◽  
Inflammatory Cytokines ◽  
Escape Latency ◽  
Neuronal Cells ◽  
Neuronal Injury ◽  
Morris Water Maze Test ◽  
Picroside Ii ◽  
Tnf Α ◽  
Pro Inflammatory Cytokines

<b><i>Introduction:</i></b> Numerous pieces of evidence demonstrated that isoflurane induces hippocampal cell injury and cognitive impairments. Picroside II has been investigated for its anti-apoptosis and antioxidant neuroprotective effects. We aimed to explore the protective effects of picroside II and the role of microRNA-195 (miR-195) on isoflurane-induced neuronal injury in rats. <b><i>Methods:</i></b> The Morris water maze test was used to evaluate the effects of isoflurane on rats regarding escape latency and time in quadrant parameters. Real-time quantitative PCR was used to detect the expression levels of miR-195 and pro-inflammatory cytokines, including inter­leukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) mRNA, in the hippocampal tissues and neuronal cells. <b><i>Results:</i></b> The picroside II significantly improves isoflurane-induced higher escape latency and lower time spent in the quadrant compared with the control rats. Picroside II also promotes cell viability and suppresses cell apoptosis of isoflurane-induced neuronal cells. Besides, picroside II suppresses the expression of pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) and miR-195 in vivo and in vitro. Furthermore, overexpression of miR-195 abrogates the effects of picroside II on the expression of pro-inflammatory cytokines. The appropriate dose of picroside II is 20 mg/kg. <b><i>Conclusion:</i></b> Picroside II could protect the nervous system possibly through inhibiting the inflammatory response in the isoflurane-induced neuronal injury of rats. The protective effect of picroside II may be achieved by downregulating the expression of miR-195 and then inhibiting the inflammatory response.

Protective effect of prion protein via the N-terminal region in mediating a protective effect on paraquat-induced oxidative injury in neuronal cells

2008 ◽  
Vol 86 (3) ◽  
pp. 653-659 ◽  
Author(s):  
Ingrid Dupiereux ◽  
Nandini Falisse-Poirrier ◽  
Willy Zorzi ◽  
Nicole T. Watt ◽  
Olivier Thellin ◽  
...  
Keyword(s):  
Protective Effect ◽  
Prion Protein ◽  
Neuronal Cells ◽  
Oxidative Injury ◽  
Terminal Region

scholarly journals The Molecular Mechanism of Endoplasmic Reticulum Stress-Induced Apoptosis in PC-12 Neuronal Cells: The Protective Effect of Insulin-Like Growth Factor I

Endocrinology ◽  
2008 ◽  
Vol 150 (1) ◽  
pp. 277-285 ◽  
Author(s):  
Cheng-Gang Zou ◽  
Xiu-Zhen Cao ◽  
Yue-Shui Zhao ◽  
Shun-Yu Gao ◽  
Shu-De Li ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Protective Effect ◽  
Er Stress ◽  
P38 Mapk ◽  
Neuronal Apoptosis ◽  
Neuronal Cells ◽  
Dependent Manner ◽  
Related Protein ◽  
Igf I ◽  
Induced Apoptosis

Endoplasmic reticulum (ER) stress has been implicated in several neurodegenerative diseases. Although CCAAT/enhancer-binding protein homologous protein (CHOP) has been shown to play a critical role in ER stress, the precise apoptosis cascade downstream of CHOP is unknown. In this report, we investigated the mechanism of ER stress-mediated apoptosis as well as the action of IGF-I in PC-12 neuronal cells. Our results demonstrated that tribbles-related protein 3 (TRB3), which is a target gene of CHOP, was responsible for tunicamycin (an ER stress inducer)-induced apoptosis. TRB3 could promote dephosphorylation of Akt in PC-12 cells. IGF-I inhibited ER stress-induced apoptosis by restoring the phosphorylation level of Akt. Both wortmannin (a phosphatidylinositide 3-kinase inhibitor) and SB 212090 (a p38 MAPK inhibitor) suppressed the protective effect of IGF-I on ER stress-induced apoptosis. Interestingly, IGF-I attenuated ER stress-mediated expression of TRB3 but not CHOP. This action of IGF-I was abolished by SB 212090 but not by wortmannin. Immunoprecipitation analysis revealed that IGF-I promoted the phosphorylation of CHOP by activating p38 MAPK, probably leading to a decrease in the transcriptional activity of CHOP. The dephosphorylation of Akt resulted in increased expression of a proapoptotic protein, p53 up-regulated modulator of apoptosis (PUMA), in a forkhead box O3a-dependent manner. Knockdown of PUMA by short hairpin RNA attenuated ER stress-mediated apoptosis. Thus, our current study indicates that both TRB3 and PUMA are critical molecules in ER stress-induced apoptosis. IGF-I effectively protects PC-12 neuronal cells against ER stress-induced apoptosis through the phosphatidylinositide 3-kinase/Akt and p38 MAPK pathways. Endoplasmic reticulum (ER) stress causes neuronal apoptosis by inducing the expression of tribbles-related protein 3 and PUMA. IGF-1 prevents neuronal apoptosis against ER stress through phosphatidylinositide 3-kinase/Akt and p38 mitogen-activated protein kinase pathways.

Hsp27 and Hsp70 administered in combination have a potent protective effect against FALS-associated SOD1-mutant-induced cell death in mammalian neuronal cells

2005 ◽  
Vol 134 (2) ◽  
pp. 256-274 ◽  
Author(s):  
Yogesh J.K. Patel ◽  
Martin D. Payne Smith ◽  
Jacqueline de Belleroche ◽  
David S. Latchman
Keyword(s):  
Cell Death ◽  
Protective Effect ◽  
Neuronal Cells ◽  
Sod1 Mutant

S9-5 Bound sulfur exerts protective effect against cytotoxicity in neuronal cells

Nitric Oxide ◽  
2014 ◽  
Vol 39 ◽  
pp. S13
Author(s):  
Yuki Ogasawara ◽  
Shin Koike ◽  
Norihiro Shibuya ◽  
Kazuyuki Ishii ◽  
Hideo Kimura
Keyword(s):  
Protective Effect ◽  
Neuronal Cells

scholarly journals 1,8-cineol attenuated Aβ25-35-induced neuron injury through inhibiting IL-6, IL-8 release and NF-κB expression

2019 ◽  
Vol 8 (1) ◽  
Author(s):  
Changliang Lu ◽  
Lin Wang ◽  
Shumei Wang ◽  
Wanzhong Li ◽  
Haijian Li ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cell Viability ◽  
Western Blotting ◽  
Cortical Neurons ◽  
Cell Injury ◽  
Neuronal Cells ◽  
Rat Cortical Neurons ◽  
Induced Neuron ◽  
Neuron Injury

Objective: To explore the protective effect of 1,8-cineol against Amyloid beta25-35 ( Aβ25-35)-induced cell injury in primary rat cortical neurons. Methods: Primary rat cortical neurons were cultured in vitro, treated with different concentrations of Aβ25-35 (2.5, 5, 10 20, 40 μM) and 1,8-cineol (1, 3, 10 μM). Cell viability of neuronal cells were detected by MTT assay and cell death were detected by lactate dehydrogenase release (LDH). The production of IL-6 and IL-8 in the supernatant were measured by ELISA assay kits. NF-κB protein expression was detected by Western blotting. Results: In primary cultured neurons, Aβ25-35 concentration dependently reduced cell viability and increased LDH release. 1,8-cineol with concentrations of 3 and 10 μM protected neuronal cells against Aβ25-35 induced cell injury for 24 h. 3 and 10 μM of 1,8-cineol also significantly decreased the levels of IL-6 and IL-8 cytokine production in the supernatant. Increased NF-κB expression was also significantly reduced by 1,8-cineol treatment evaluated by Western blotting. Conclusions: Our results revealed a protective effect of 1,8-cineol on Aβ25-35 induced neuron injury through inhibition of IL-6, IL-8 production and NF-κB expression.

Sign in / Sign up

Export Citation Format

Share Document