Reversal of Trimethyltin‐Induced Learning and Memory Deficits by 3,5‐Dicaffeoylquinic Acid

Kang, Jin Yong; Park, Seon Kyeong; Guo, Tian; Ha, Jeong Su; Lee, Du Sang; Kim, Jong Min; Lee, Uk; Kim, Dae‐Ok; Heo, Ho Jin

doi:10.1155/2016/6981595

Cited by 51 publications

(56 citation statements)

References 37 publications

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“…Therefore, in this study, we induced the oxidative stress injury in H9C2 by using TBHP, which is one of the most common oxidizing agents in experiments ( 28 ). In this study, we found that 3,5-diCQA showed a protective effect on H9C2 cells with an improvement of cell viability in a dose-dependent manner, which is in agreement with previous researches ( 26 , 27 ). These results demonstrated that 3,5-diCQA inhibits oxidative stress-induced apoptosis in H9C2.…”

Section: Discussionsupporting

confidence: 93%

“…It has been reported that 3,5-diCQA attenuated caspase-3 activation induced by H 2 O 2 , causing an increase in survival of SH-SY5Y cells in vitro ( 14 ). Consistently, 3,5-diCQA may prevent neuronal apoptosis through the repression of apoptotic signaling molecules such as Bax in vivo ( 26 ). In this study, we found that 3,5-diCQA was indeed able to reduce apoptosis induced by TBHP in H9C2 cells by improving the ratio of Bcl-2 to Bax and descending cleaved caspase-3, indicating that 3,5-diCQA inhibits apoptosis by suppression of the mitochondria-mediated intrinsic apoptosis pathway.…”

Section: Discussionmentioning

confidence: 90%

“…Inhibition of cardiomyocyte apoptosis contributes to ameliorating the failing myocardium and is the basis for therapy for HF ( 23 , 24 ). 3,5-diCQA, a common derivative of coffee, was found to protect neuronal cells in neurodegenerative diseases implicated with oxidative stress ( 25 , 26 ). A previous study also found that 3,5-diCQA possesses a cytoprotective effect against H 2 O 2 -induced oxidative stress on SH-SY5Y cells ( 27 ).…”

Section: Discussionmentioning

confidence: 99%

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3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway

Bi¹,

Wu²,

Chen³

et al. 2018

Food & Nutrition Research

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BackgroundOxidative stress-induced apoptosis plays an important role in the development of heart failure. 3,5-Dicaffeoylquinic acid (3,5-diCQA), a phenolic compound, has shown protective effects against oxidative stress in many diseases.ObjectiveThe objective of this study was to investigate the anti-apoptosis potential of 3,5-diCQA in cardiomyocyte cells under oxidative stress and explore its underlying mechanisms.DesignA model of tert-butyl hydroperoxide (TBHP)-induced apoptosis in a cardiomyocyte cell line (H9C2) was established. Cell viabilities on cell lines were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium (MTT) assay. The apoptosis was measured by hoechst33342 and propidium iodide (PI) fluorescent staining. PI (in red) stained the regions of cell apoptosis; Hoechet33342 (in blue) stained the nuclei. The Western blot was used to determine the expressions of related proteins such as p-PI3K: phosphorylated phosphatidylinositol-3-kinase (p-PI3K), phosphorylated Serine and Threonine kinase AKT (p-AKT), p-PTEN, Bcl-2, Bax, and caspase-3. Afterward, a PI3K inhibitor, LY294002, was applied to confirm the influence of the PI3K/Akt pathway on TBHP-treated cells of 3,5-diCQA. Then, H9C2 cells were pre-incubated with 3,5-diCQA alone to determine if the expression of activated PI3K/Akt signaling was mediated by 3,5-diCQA in H9C2 cells.ResultsThe results showed that TBHP resulted in an increase in cardiomyocyte apoptosis, whereas 3,5-diCQA treatment protected cells from TBHP-induced apoptosis in a dose-dependent manner. Moreover, 3,5-diCQA decreased expressions of Bax and caspase-3 but increased the phosphorylation levels of PI3K and Akt in TBHP-treated cells, which are the key molecules mediating cell survival, whereas phosphatase and tensin homologue deleted on chromosome 10 (PTEN) phosphorylation was unchanged. Importantly, pre-incubation with a PI3K inhibitor (LY294002) partly abolished the anti-apoptosis effects of 3,5-diCQA. Further, 3,5-diCQA enhanced the phosphorylation levels of PI3K and Akt in H9C2 cells directly, while LY294002 attenuated the effects of 3,5-diCQA on PI3K and Akt.ConclusionThis study suggested that 3,5-diCQA rescued myocardium from apoptosis by increasing the activation of the PI3K/Akt signaling pathway.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 90%

Section: Discussionmentioning

confidence: 99%

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3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway

Bi¹,

Wu²,

Chen³

et al. 2018

Food & Nutrition Research

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“…Moreover, 3.5-Dicaffeoylquinic acid was identified as a major component of Artemisia annua L. in an LC–negative ion ESI-MS total ion current (TIC) profile [ 33 ]. In our previous research, 3.5-Dicaffeoylquinic acid was analyzed by a Q-TOF MS system in ESI-negative mode and found to be a main phenolic compound of Artemisia argyi H. ethyl acetate fractions [ 34 ]. In other words, these results suggest that the physiological activity could be affected by components changed by Monascus purpureus fermentation.…”

Section: Resultsmentioning

confidence: 99%

Cognitive Function of Artemisia argyi H. Fermented by Monascus purpureus under TMT‐Induced Learning and Memory Deficits in ICR Mice

Kang

Lee

Park

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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The cognitive effect of Artemisia argyi H. under liquid-state fermentation by Monascus purpureus (AAFM), which has cellular antioxidant activity and neuronal cell viability, on trimethyltin- (TMT-) induced learning and memory impairment in Institute of Cancer Research (ICR) mice was confirmed. Tests were conducted to determine the neuroprotective effects against H2O2-induced oxidative stress, and the results showed that AAFM has protective effects through the repression of mitochondrial injury and cellular membrane damage against H2O2-induced neurotoxicity. In animal experiments, such as the Y-maze, passive avoidance, and Morris water maze tests, AAFM also showed excellent ameliorating effects on TMT-induced cognitive dysfunction. After behavioral tests, brain tissues were extracted to assess damage to brain tissue. According to the experimental results, AAFM improved the cholinergic system by upregulating acetylcholine (ACh) contents and inhibiting acetylcholinesterase (AChE) activity. AAFM effectively improved the decline of the superoxide dismutase (SOD) level and the increase of the oxidized glutathione (GSH) ratio and lipid peroxidation (malondialdehyde (MDA) production) caused by TMT-induced oxidative stress. The occurrence of mitochondrial dysfunction and apoptosis was also decreased compared with the TMT group. Finally, quinic acid derivatives were identified as the major phenolic compounds in AAFM using ultra-performance liquid chromatography quadrupole-time-of-flight (UPLC-Q-TOF) MS analysis.

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“…Artemisia argyi is also one of the mugworts, and recently, its various physiological activities have been confirmed. In our previous research, it was confirmed that 3,5-dicaffeoylquinic acid (3,5-diCQA) and 4,5-diCQA were abundant in Artemisia argyi (Kang et al, 2016). 3,5-diCQA and 4,5-diCQA are isomers of diC-QAs, and they have superior antioxidant activity over chlorogenic acid, which is a well-known antioxidant.…”

mentioning

confidence: 78%

4,5‐dicaffeyolquinic acid improves high‐fat diet‐induced cognitive dysfunction through the regulation of insulin degrading enzyme

et al. 2019

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This study was performed to investigate the effects of Artemisia argyi and 4,5‐dicaffeyolquinic acid (4,5‐diCQA) as a main compound of ethyl acetate fraction from Artemisia argyi (EFAA) on high‐fat diet (HFD)‐induced cognitive dysfunction. Both EFAA and 4,5‐diCQA were effective in improving cognitive function on HFD‐induced cognitive dysfunction. In brain tissue analysis, it was confirmed that EFAA and 4,5‐diCQA inhibited the reduction of neurotransmitters as well as oxidative stress and mitochondrial dysfunction. In addition, they inhibited amyloid β (Aβ) accumulation by increasing the expression of insulin‐degrading enzyme and consequently prevented apoptosis. In conclusion, it is presumed that Artemisia argyi may help to improve the cognitive impairment due to the HFD, and it is considered that this effect is closely related to the physiological activity of 4,5‐diCQA. Practical applications Artemisia argyi is used in traditional herbal medicine in Asia. Type 2 diabetes mellitus has been proven by a variety of epidemiological studies to be a risk factor for cognitive impairment, such as Alzheimer’s disease. This study confirmed that 4,5‐diCQA is a bioactive compound of Artemisia argyi on improving HFD‐induced cognitive dysfunction. Therefore, this study can provide useful information to the effect of Artemisia argyi and related substance.

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Reversal of Trimethyltin‐Induced Learning and Memory Deficits by 3,5‐Dicaffeoylquinic Acid

Cited by 51 publications

References 37 publications

3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway

3,5-Dicaffeoylquinic acid protects H9C2 cells against oxidative stress-induced apoptosis via activation of the PI3K/Akt signaling pathway

Cognitive Function of Artemisia argyi H. Fermented by Monascus purpureus under TMT‐Induced Learning and Memory Deficits in ICR Mice

4,5‐dicaffeyolquinic acid improves high‐fat diet‐induced cognitive dysfunction through the regulation of insulin degrading enzyme

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