Protective effect of Toki-shakuyaku-san on amyloidβ25-35-induced neuronal damage in cultured rat cortical neurons

2005 ◽  
Vol 19 (5) ◽  
pp. 450-453 ◽  
Author(s):  
Nobuaki Egashira ◽  
Katsunori Iwasaki ◽  
Yuki Akiyoshi ◽  
Yuki Takagaki ◽  
Izzettin Hatip-Al-Khatib ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cortical Neurons ◽  
Neuronal Damage ◽  
Rat Cortical Neurons

scholarly journals The Protective Effect of Rho-Associated Kinase Inhibitor on Aluminum-Induced Neurotoxicity in Rat Cortical Neurons

2010 ◽  
Vol 116 (1) ◽  
pp. 264-272 ◽  
Author(s):  
Tsan-Ju Chen ◽  
Hui-Shan Hung ◽  
Dean-Chuan Wang ◽  
Shun-Sheng Chen
Keyword(s):  
Protective Effect ◽  
Cortical Neurons ◽  
Kinase Inhibitor ◽  
Rat Cortical Neurons

Protective effect of erythropoietin against ketamine-induced apoptosis in cultured rat cortical neurons: Involvement of PI3K/Akt and GSK-3 beta pathway

APOPTOSIS ◽  
2007 ◽  
Vol 12 (12) ◽  
pp. 2187-2195 ◽  
Author(s):  
You Shang ◽  
Yan Wu ◽  
Shanglong Yao ◽  
Xiaojing Wang ◽  
Dan Feng ◽  
...  
Keyword(s):  
Protective Effect ◽  
Cortical Neurons ◽  
Rat Cortical Neurons ◽  
Induced Apoptosis

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.

Protective effect of donepezil in primary-cultured rat cortical neurons exposed to N-methyl-d-aspartate (NMDA) toxicity

2006 ◽  
Vol 530 (3) ◽  
pp. 215-222 ◽  
Author(s):  
Shigeru Akasofu ◽  
Manami Kimura ◽  
Takashi Kosasa ◽  
Hiroo Ogura ◽  
Kohei Sawada
Keyword(s):  
Protective Effect ◽  
Cortical Neurons ◽  
Rat Cortical Neurons

scholarly journals Lycopus lucidus Turcz exerts neuroprotective effect against H2O2‑induced neuroinflammation by inhibiting NLRP3 inflammasome activation in cortical neurons

2021 ◽  
Author(s):  
Hyunseong Kim ◽  
Jin Young Hong ◽  
Wan-Jin Jeon ◽  
Junseon Lee ◽  
Seung Ho Baek ◽  
...  
Keyword(s):  
Cell Death ◽  
Nlrp3 Inflammasome ◽  
Cortical Neurons ◽  
Neuronal Damage ◽  
Neuroprotective Effect ◽  
Synaptic Connectivity ◽  
Inflammasome Activation ◽  
Caspase 1 ◽  
Nlrp3 Inflammasome Activation ◽  
Rat Cortical Neurons

Abstract Background Central nervous system (CNS) injuries are a leading cause of permanent functional impairment in humans. Nerve damage can be aggravated by neuroinflammation mediated by protein complexes known as inflammasomes, such as the NLRP3 inflammasome which is a key mediator of caspase-1 and interleukin-1β (IL-1β) /interleukin-18 (IL-18) activation. Lycopus lucidus Turcz (LLT) is a traditional medicinal herb that exerts therapeutic effects against oxidative stress, inflammation, and angiogenesis; however, it remains unclear whether LLT can directly protect neurons against damage, and the underlying molecular mechanisms are poorly understood. Methods We investigated the neuroprotective effect of LLT against hydrogen peroxide (H2O2)-induced neuronal damage in cultured primary rat cortical neurons, as well as the potential underlying mechanisms. Neuronal viability and cell death assays were used to determine the effects of LLT on neuroprotection, while the mode of cell death was confirmed using flow cytometry. Changes in the expression of inflammatory factors involved in activation of the NLRP3 inflammasome were measured using immunocytochemistry (ICC) and confirmed by real-time PCR. And, we analyzed that the effect of LLT on neurotrophic factors secretion and synaptic connectivity using ICC in H2O2-induced neuron at 7 days in vitro. Results LLT effectively protected cultured rat cortical neurons from H2O2-induced injury by significantly inhibiting NLRP3 inflammasome activation. In addition, LLT significantly reduced caspase1 activation, which is known to be induced by inflammasome formation, and consequently regulated the secretion of IL-1β/IL-18. We demonstrated that LLT enhances axonal elongation and synaptic connectivity against H2O2-induced injury of rat primary cortical neuron. Conclusions Together, these results demonstrate that LLT can directly protect cultured cortical neurons from H2O2-induced neuronal damage by inhibiting NLRP3 inflammasome activation and the secretion of caspase-1 and IL-1β/IL-18. Thus, our study provides new insights into the therapeutic mechanisms of LLT and suggests that the NLRP3 inflammasome could be a promising target for treating neurological diseases.

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