Neuroprotective effects of artemisinin against isoflurane-induced cognitive impairments and neuronal cell death involve JNK/ERK1/2 signalling and improved hippocampal histone acetylation in neonatal rats

Xu, Guang; Huang, Yiqin; Li, Ping-le; Guo, Haiming; Han, Xiuxin

doi:10.1111/jphp.12704

Cited by 24 publications

(16 citation statements)

References 57 publications

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“…In experimental animal models, isoflurane brings about mitochondrial dysfunction, neuroinflammation, and apoptosis, leading to cognitive impairments and neuronal cell death (Li et al, 2014; Hu X. et al, 2017; Liang et al, 2017; Su et al, 2017; Wu et al, 2017; Xu et al, 2017). Furthermore, it has been observed to modulate glutamate receptors.…”

Section: Glutamate Receptors As Potential Targets In Neurotoxic Agentmentioning

confidence: 99%

“…Furthermore, it has been observed to modulate glutamate receptors. One study has reported that NMDAR-mediated excitatory synaptic transmission is more sensitive to isoflurane than non-NMDAR-mediated excitatory synaptic transmission (Xu et al, 2017). In addition, at minimum alveolar concentrations, isoflurane causes GABA A receptor antagonism and increases NMDARs inhibition (Nishikawa and MacIver, 2000).…”

Section: Glutamate Receptors As Potential Targets In Neurotoxic Agentmentioning

confidence: 99%

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Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Jakaria

Park

Haque

et al. 2018

Front. Mol. Neurosci.

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Glutamate receptors play a crucial role in the central nervous system and are implicated in different brain disorders. They play a significant role in the pathogenesis of neurodegenerative diseases (NDDs) such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. Although many studies on NDDs have been conducted, their exact pathophysiological characteristics are still not fully understood. In in vivo and in vitro models of neurotoxic-induced NDDs, neurotoxic agents are used to induce several neuronal injuries for the purpose of correlating them with the pathological characteristics of NDDs. Moreover, therapeutic drugs might be discovered based on the studies employing these models. In NDD models, different neurotoxic agents, namely, kainic acid, domoic acid, glutamate, β-N-Methylamino-L-alanine, amyloid beta, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, 1-methyl-4-phenylpyridinium, rotenone, 3-Nitropropionic acid and methamphetamine can potently impair both ionotropic and metabotropic glutamate receptors, leading to the progression of toxicity. Many other neurotoxic agents mainly affect the functions of ionotropic glutamate receptors. We discuss particular neurotoxic agents that can act upon glutamate receptors so as to effectively mimic NDDs. The correlation of neurotoxic agent-induced disease characteristics with glutamate receptors would aid the discovery and development of therapeutic drugs for NDDs.

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Section: Glutamate Receptors As Potential Targets In Neurotoxic Agentmentioning

confidence: 99%

Section: Glutamate Receptors As Potential Targets In Neurotoxic Agentmentioning

confidence: 99%

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Jakaria

Park

Haque

et al. 2018

Front. Mol. Neurosci.

View full text Add to dashboard Cite

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“…In another study, clinically relevant concentrations of artemisinin were demonstrated to protect and rescue neuronal PC12 cells from the cell death induced by amyloid beta-peptide 25–35 (Aβ 25-35 ), during which artemisinin was verified to act as a neuronal protectant from Aβ 25-35 insult via activation of the ERK1/2 pathway ( Zeng Z. et al, 2017 ). Furthermore, the neuroprotective effect of artemisinin was assessed by the exposure of neonatal rats to the neurotoxin isoflurane, and artemisinin was found to exhibit an inhibitory effect on isoflurane-induced neuronal cell death and ameliorate cognitive impairment and memory loss by modulating histone acetylation and signal transduction through the c-Jun N-terminal kinase (JNK) and ERK1/2 pathways ( Xu G. et al, 2017 ).…”

Section: Artemisinin Targets Receptors Impacting On Signaling Cascadementioning

confidence: 99%

Artemisinin: A Panacea Eligible for Unrestrictive Use?

et al. 2017

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Although artemisinin has been used as anti-malarial drug, accumulating evidence on the extended therapeutic potential of artemisinin emerges. Apart from anti-malaria and anti-tumor, artemisinin can also exert beneficial effects on some metabolic disorders, such as obesity, diabetes, and aging-related diseases. However, whether artemisinin should be applied to treatment of the wide-spectrum diseases is debating. Here, we discuss the predisposition of a raised risk of malarial resistance to artemisinin from consideration of the multi-target and non-specific features of artemisinin.

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“…These identified genes were also related to a list of Gene Ontology (GO) terms and the Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. For example, the pathways involve "complement and coagulation cascades," which have been reported to play important roles in the progression of DKD (Wang et al, 2016c), and the "p53 signaling pathway" and "TGF-β signaling pathway," which are closely associated with DKD (Zhang et al, 2011;Wang et al, 2016a;Mukhi et al, 2017;Xu et al, 2017a;Shelbaya et al, 2018;Sheng et al, 2018;Xiang et al, 2019). These results indicate promising targets in the treatment of DKD with artemisinins.…”

Section: Type 2 Diabetes Mellitus-related Complications Diabetic Kidnmentioning

confidence: 88%

The Potential Roles of Artemisinin and Its Derivatives in the Treatment of Type 2 Diabetes Mellitus

et al. 2020

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Type 2 diabetes mellitus (T2DM) is a chronic disease that has become a global public health problem. Studies on T2DM prevention and treatment mostly focus on discovering therapeutic drugs. Artemisinin and its derivatives were originally used as antimalarial treatments. In recent years, the roles of artemisinins in T2DM have attracted much attention. Artemisinin treatments not only attenuate insulin resistance and restore islet ß-cell function in T2DM but also have potential therapeutic effects on diabetic complications, including diabetic kidney disease, cognitive impairment, diabetic retinopathy, and diabetic cardiovascular disease. Many in vitro and in vivo experiments have confirmed the therapeutic utility of artemisinin and its derivatives on T2DM, but no article has systematically demonstrated the specific role artemisinin plays in the treatment of T2DM. This review summarizes the potential therapeutic effects and mechanism of artemisinin and its derivatives in T2DM and associated complications, providing a reference for subsequent related research.

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Neuroprotective effects of artemisinin against isoflurane-induced cognitive impairments and neuronal cell death involve JNK/ERK1/2 signalling and improved hippocampal histone acetylation in neonatal rats

Abstract: Artemisinin effectively inhibited neuronal apoptosis and improved cognition and memory via regulating histone acetylation and JNK/ERK1/2 signalling.

Cited by 24 publications

References 57 publications

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Neurotoxic Agent-Induced Injury in Neurodegenerative Disease Model: Focus on Involvement of Glutamate Receptors

Artemisinin: A Panacea Eligible for Unrestrictive Use?

The Potential Roles of Artemisinin and Its Derivatives in the Treatment of Type 2 Diabetes Mellitus

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