Protective Effects of Costunolide against Hydrogen Peroxide-Induced Injury in PC12 Cells

Cheong, Chong-Un; Yeh, Ching-Sheng; Hsieh, Ya Ching; Lee, Ying‐Ray; Lin, Ming‐Fong; Chen, Chung‐Yi; Lee, Chien-Hsing

doi:10.3390/molecules21070898

Cited by 37 publications

(23 citation statements)

References 42 publications

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“…Oxidative stress-mediated cellular injury is a major cause of neurodegenerative diseases, and PC-12 cells have been applied for model construction in analysing the molecular mechanism of SCI in vitro [21][22][23]. Moreover, SCI is reported as a fearful neurology-related disease and the latent therapeutic strategies for this injury have been grabbed in PC-12 cells [24].…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Overexpression of lncRNA ANRIL aggravated hydrogen peroxide-disposed injury in PC-12 cells via inhibiting miR-499a/PDCD4 axis-mediated PI3K/Akt/mTOR/p70S6K pathway

Guo

Gao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Spinal cord injury (SCI) is a grievous neurology-related disorder that causes many devastating symptoms. This research planned to dig the function and latent mechanisms of long noncoding RNA (lncRNA) ANRIL on hydrogen peroxide (H 2 O 2)-disposed injury in PC-12 cells. The PC-12 cells were disposed with H 2 O 2 for 24 h to construct the SCI model. H 2 O 2-disposed PC-12 cells was assessed by detecting cell viability, migration, invasion, apoptosis and autophagy. The level of ANRIL in H 2 O 2-disposed PC-12 cells was analysed, afterwards, the impacts of ANRIL silencing on H 2 O 2-disposed PC-12 cell injury was determined. The regulatory association between ANRIL and miR-499a, between miR-499a and PDCD4, as well as PDCD4 and PI3K/Akt/mTOR/p70S6K signals were investigated. H 2 O 2 produced PC-12 cell injury and promoted the level of ANRIL. Silencing of ANRIL inhibited H 2 O 2-disposed PC-12 cell injury through promoting cell viability, migration, invasion and inhibiting apoptosis and autophagy. Moreover, miR-499a was upregulated after silencing of ANRIL, and inhibition of miR-499a reversed the effects of silencing of ANRIL on H 2 O 2-disposed PC-12 cell injury. Also, PDCD4 was a target of miR-499a. Furthermore, ANRIL silencing alleviated the H 2 O 2-disposed injury in PC-12 cells possible by activating PI3K/Akt/mTOR/p70S6K signals, which was mediated by miR-499a/PDCD4 axis. Our results indicate that high level of ANRIL may sharpen the degree of SCI via targeting miR-499a/PDCD4 axis to regulate the briskness of PI3K/Akt/mTOR/p70S6K signals.

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Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Overexpression of lncRNA ANRIL aggravated hydrogen peroxide-disposed injury in PC-12 cells via inhibiting miR-499a/PDCD4 axis-mediated PI3K/Akt/mTOR/p70S6K pathway

Guo

Gao

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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“…In ancient times, people thought the root of this plant has the function of promoting the circulation of blood and relieving pain [8]. It was reported that costunolide could inhibits proliferation, arrests cell cycle and induces apoptosis of many cancers, such as breast cancer, colon cancer, bladder cancer, prostate cancer and hepatocellular carcinoma cells [9][10][11][12][13][14][15][16][17]. However, the research on GC inhibited by costunolide is relatively few.…”

Section: Introductionmentioning

confidence: 99%

Costunolide induces mitochondria-mediated apoptosis in human gastric adenocarcinoma BGC-823 cells

Yan

et al. 2019

BMC Complement Altern Med

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Background: Costunolide, a sesquiterpene lactone extracted from Radix Aucklandiae, has the activity against multiple cancers. However, the effect of costunolide on gastric cancer (GC) have remained to be ambiguous. In this study, we investigated the underlying mechanisms of apoptosis induced by costunolide in human gastric adenocarcinoma BGC-823 cells in vitro and in vivo. Methods: The viability of BGC-823 cells was detected by MTT assay. The apoptosis and mitochondrial membrane potential (ΔΨm) of BGC-823 cells induced by costunolide were analyzed by flow cytometry. The inhibiton of costunolide on human gastric adenocarcinoma was estimated in xenografts in nude mice. Apoptosis related proteins and genes were detected by Western blot and Q-PCR. Results: Costunolide inhibited the viability of BGC-823 cells in a time and concentration dependent manner. Costunolide induced the apoptosis and lowered the ΔΨm of BGC-823 cells significantly. Costunolide increased the expression of Bax, cleaved caspase 9, cleaved caspase 7, cleaved caspase 3 and cleaved poly ADP ribose polymerase (PARP) proteins and decreased the expression of Bcl-2, pro-caspase 9, pro-caspase 7, pro-caspase 3 and PARP proteins. Costunolide upregulated the expression of puma, Bak1 and Bax mRNA and downregulated the expression of Bcl-2 mRNA. In addition, we demonstrated that costunolide inhibited the growth and induced apoptosis of BGC-823 cells xenografted in athymic nude mice. Costunolide increased the expression of cleaved caspase 9, cleaved caspase 3 and Bax proteins and decreased the expression of Bcl-2 protein in xenografted tumor. Costunolide upregulated the expression of puma and Bax mRNA and decreased the expression of Bcl-2 mRNA in xenografted tumor. Conclusions: Collectively, our results suggested that costunolide induced mitochondria-mediated apoptosis in human gastric adenocarcinoma BGC-823 cells and could be the candidate drug against GC in clinical practice.

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“…PC12 cells, which derive from a rat pheochromocytoma and possess neuron-like characteristics, have been applied for construction of useful model system in analyzing the neurological apoptosis [19]. SCI is a severe neurological disease, and mounting researches have used PC12 cells as important adjuncts and surrogates for studies of SCI in humans [20,21].…”

Section: Original Papermentioning

confidence: 99%

Chinese Angelica Polysaccharide (CAP) Alleviates LPS-Induced Inflammation and Apoptosis by Down-Regulating COX-1 in PC12 Cells

Xie

Zhang

et al. 2018

Cell Physiol Biochem

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Background/Aims: Chinese angelica polysaccharide (CAP) is the main effective ingredient of angelica sinensis and exerts anti-inflammatory and anti-apoptotic effects on many diseases. This study aimed to explore the pharmacological potential of CAP on spinal cord injury (SCI). Methods: PC12 cells were pretreated by CAP and were subjected to LPS. Transfection was performed to alter the expression of COX-1. Cell viability and apoptotic cell rate were measured by CCK-8 and flow cytometry respectively. qRT-PCR and western blot analysis were performed to assess the expression changes of pro-inflammatory cytokines, apoptosis-related factor and core kinases in PI3K/AKT pathway. Results: LPS stimulation induced significant cell damage in PC12 cells as cell viability was repressed, apoptosis was induced and the expression levels of IL-1β, IL-6, IL-8, and TNF-α were increased. CAP pretreatment protected PC12 cells against LPS-induced cell damage. Meanwhile CAP treatment reduced the expression of COX-1 even in LPS-stimulated PC12 cells. More importantly, COX-1 overexpression abolished the protective effects of CAP on LPS-injured PC12 cells. Finally, Western blot analytical results showed that CAP activated PI3K/AKT pathway also in a COX-1-dependent manner. Conclusion: CAP exerted anti-apoptotic and anti-inflammatory effects on LPS-injured PC12 cells via down-regulation of COX-1.

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Protective Effects of Costunolide against Hydrogen Peroxide-Induced Injury in PC12 Cells

Cited by 37 publications

References 42 publications

RETRACTED ARTICLE: Overexpression of lncRNA ANRIL aggravated hydrogen peroxide-disposed injury in PC-12 cells via inhibiting miR-499a/PDCD4 axis-mediated PI3K/Akt/mTOR/p70S6K pathway

RETRACTED ARTICLE: Overexpression of lncRNA ANRIL aggravated hydrogen peroxide-disposed injury in PC-12 cells via inhibiting miR-499a/PDCD4 axis-mediated PI3K/Akt/mTOR/p70S6K pathway

Costunolide induces mitochondria-mediated apoptosis in human gastric adenocarcinoma BGC-823 cells

Chinese Angelica Polysaccharide (CAP) Alleviates LPS-Induced Inflammation and Apoptosis by Down-Regulating COX-1 in PC12 Cells

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