Tanshinone IIA Inhibits Glutamate‐Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH‐SY5Y Human Neuroblastoma Cells

Li, Haifeng; Han, Wenjing; Wang, Hongyu; Ding, Fei; Xiao, Lingyun; Shi, Ruona; Ai, Liping; Huang, Zebo

doi:10.1155/2017/4517486

Cited by 43 publications

(45 citation statements)

References 60 publications

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“…Tanshinone IIA is a natural diterpene quinone isolated from the roots of Salvia miltiorrhiza Bunge that has been used as a traditional Chinese medicine for promotion of blood circulation and relieving vessel stasis [ 20 ]. Previous studies have further shown that tanshinone IIA is effective for treating coronary, cerebrovascular, and cardiovascular diseases [ 21 , 22 , 23 ].…”

Section: Introductionmentioning

confidence: 99%

Anti-Adipogenic Effects on 3T3-L1 Cells and Zebrafish by Tanshinone IIA

Park

Obiang-Obounou

Lee

et al. 2017

IJMS

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Tanshinone IIA is a diterpene quinone isolated from the roots of Salvia miltiorrhiza bunge that has traditionally been used in China for the treatment of cardiovascular and cerebrovascular disorders. Although there is recent evidence showing that tanshinone IIA has an anti-obesity effect, its underlying mechanism of anti-obesity effect is poorly understood. Here, we investigated the effect of tanshinone IIA on lipid accumulation in 3T3-L1 preadipocytes and zebrafish. Notably, tanshinone IIA at 10 μM concentration greatly reduced lipid accumulation and triglyceride (TG) contents during 3T3-L1 preadipocyte differentiation, suggesting its anti-adipogenic effect. On mechanistic levels, tanshinone IIA reduced the expression levels of CCAAT/enhancer-binding protein-α (C/EBP-α), peroxisome proliferator-activated receptor-γ (PPAR-γ), fatty acid synthase (FAS), and perilipin A but also the phosphorylation levels of signal transducer and activator of transcription-3/5 (STAT-3/5) in differentiating 3T3-L1 cells. In addition, tanshinone IIA strongly inhibited leptin and resistin mRNA expression in differentiating 3T3-L1 cells. Importantly, the tanshinone IIA’s lipid-reducing effect was also seen in zebrafish. In sum, these findings demonstrate that tanshinone IIA has anti-adipogenic effects on 3T3-L1 cells and zebrafish, and its anti-adipogenic effect on 3T3-L1 cells is largely attributable to the reduced expression and/or phosphorylation levels of C/EBP-α, PPAR-γ, FAS, perilipin A, and STAT-3/5.

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Section: Introductionmentioning

confidence: 99%

Anti-Adipogenic Effects on 3T3-L1 Cells and Zebrafish by Tanshinone IIA

Park

Obiang-Obounou

Lee

et al. 2017

IJMS

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“…The antioxidant characteristics of achillolide A demonstrated in this study in Aβ-treated N2a neuroblastoma cells support our previous observations, showing similar effects in glutamate-treated neuroblastoma N2a cells [ 22 ], H 2 O 2 -treated astrocytes and LPS-activated microglial cells [ 20 , 24 ]. Although part of Aβ toxicity is mediated by glutamate [ 27 ], the mechanism underlying Aβ cytotoxicity is complex and involves many downstream targets (for review see [ 28 ]). As neuronal vulnerability in AD originates in the hippocampal formation, future experiments should examine the effect of achillolide A on these neuronal populations in vitro and in vivo.…”

Section: Resultsmentioning

confidence: 99%

β-amyloid cytotoxicity is prevented by natural achillolide A

et al. 2018

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Alzheimer’s disease (AD) is the most prevalent cause of dementia in adults. Current available drugs for AD transiently alleviate some of the symptoms, but do not modify the disease mechanism or cure it. Therefore, new drugs are desperately needed. Key contributors to AD are amyloid beta (Aβ)- and reactive oxygen species (ROS)-induced cytotoxicities. Plant-derived substances have been shown to affect various potential targets in various diseases including AD. Therefore, phytochemicals which can protect neuronal cells against these insults might help in preventing and treating this disease. In the following research, we have isolated the sesquiterpene lactone achillolide A from the plant Achillea fragrantissima and, for the first time, characterized its effects on Aβ-treated neuroblastoma cells. Aβ is a peptide derived from the sequential cleavage of amyloid precursor protein, and is part of the pathogenesis of AD. Our current study aimed to determine whether achillolide A can interfere with Aβ-induced processes in Neuro2a cells, and protect them from its toxicity. Our results show that achillolide A decreased Aβ-induced death and enhanced the viability of Neuro2a cells. In addition, achillolide A reduced the accumulation of Aβ-induced ROS and inhibited the phosphorylation of stress-activated protein kinase/c-Jun N-terminal kinase and p44/42 mitogen-activated protein kinase in these cells. We therefore suggest that achillolide A may have therapeutic potential for the treatment of AD.

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“…We have showed that the PMV-CD36 complex activates MKK4/JNK2 signals and contributes to platelet activation [11]. Earlier studies demonstrated that TS IIA can reduce oxidative stress and regulate apoptosis by suppressing JNK and p38 MAPK activation [19]. Nevertheless, the effect of TS IIA on platelet MAPK signal pathways is unknown.…”

Section: Discussionmentioning

confidence: 98%

Tanshinone IIA prevents platelet activation and down-regulates CD36 and MKK4/JNK2 signaling pathway

Wang

Zhong

et al. 2020

BMC Cardiovasc Disord

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Background: Tanshinone IIA (TS IIA), a multi-pharmaceutical compound from traditional Chinese herb, is effective for treatment of atherothrombosis. However, the underlying mechanisms of TS IIA-mediated anti-platelet activation effect are still poorly understood. As shown in our previous study, platelet-derived microvesicles (PMVs) generated in response to oxidant insult could activate CD36/mitogen-activated protein kinase kinase 4/Jun N-terminal kinase 2 (CD36/MKK4/JNK2) signals and lead to platelet activation. The present study aims to investigate the effect of TS IIA on platelet activation and the possible mechanisms. Methods: The production of PMVs induced by Interleukin 6 (IL-6) was detected by flow cytometry. We performed activating studies of platelets with PMVs derived from IL-6-treated platelets (IL-6-PMVs) in vitro. Sometimes, platelet suspensions were incubated with serial concentrations of TS IIA for 15 min before being stimulated with IL-6-PMVs. Expression of platelet integrin α IIb β 3 and CD36 was detected by flow cytometry. Phosphorylation of MKK4 and JNK were detected by immunoblotting. Results: Here we demonstrated firstly that TS IIA could prevent platelet activation induced by PMVs and downregulates CD36 and MKK4/JNK2 signaling pathway. CD36 may be the target of atherosclerosis (AS)-related thrombosis. Conclusions: This study showed the possible mechanisms of TS IIA-mediated anti-platelet activation and may provide a new strategy for the treatment of AS-related thrombosis by targeting platelet CD36.

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Tanshinone IIA Inhibits Glutamate‐Induced Oxidative Toxicity through Prevention of Mitochondrial Dysfunction and Suppression of MAPK Activation in SH‐SY5Y Human Neuroblastoma Cells

Cited by 43 publications

References 60 publications

Anti-Adipogenic Effects on 3T3-L1 Cells and Zebrafish by Tanshinone IIA

Anti-Adipogenic Effects on 3T3-L1 Cells and Zebrafish by Tanshinone IIA

β-amyloid cytotoxicity is prevented by natural achillolide A

Tanshinone IIA prevents platelet activation and down-regulates CD36 and MKK4/JNK2 signaling pathway

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