MiR-25 protects PC-12 cells from H<sub>2</sub>O<sub>2</sub>mediated oxidative damage via WNT/β-catenin pathway

Guo, Yi; Niu, Shizhen

doi:10.1080/10790268.2017.1336319

Cited by 20 publications

(9 citation statements)

References 40 publications

(38 reference statements)

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“…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]. Therefore, in this study, we investigated the protective effects of CAP against LPS-induced injuries in PC12 cells and explored its underlying molecular mechanisms.…”

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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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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“…Currently, drug and surgical treatments are the main therapeutic strategies for SCI [5], nevertheless, the side effects of these treatments are inevitable. In various researches, local oxidative damage has been reported to occur after SCI [6,7]. It has been discovered that accelerations of reactive oxygen species (ROS) and oxidative stress are deemed to the paramount events in SCI [8].…”

Section: Introductionmentioning

confidence: 99%

Protective functions of salvianolic acid B in PC-12 cells against hydrogen peroxide-triggered damage by mediation of microRNA-26a

Liu

Fan

2019

Artificial Cells, Nanomedicine, and Biotechnology

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Spinal cord injury (SCI) can lead to varying degrees of sensory and motor dysfunction. Salvianolic acid B (Sal-B) is the dominating bioactive constituent of Danshen, which has been reported to alleviate liver fibrosis and exert neuroprotective effects. But, the influence of Sal-B in SCI remains mysterious. The research planned to delve the protective function of Sal-B in hydrogen peroxide (H 2 O 2)-caused PC-12 cell injury. H 2 O 2-caused PC-12 cells injury model was built, CCK-8, Transwell and flow cytometry experiments were enforced to assess cell proliferation, migration and apoptosis. The microRNA (miR)-26a plasmid and the matching control were transfected into PC-12 cells, subsequently, the influence of miR-26a inhibition in H 2 O 2-corrupted PC-12 cells was evaluated. The cell growth-correlated factors and PI3K/AKT and MEK/ERK pathways were assayed through western blot assay. Results corroborated that Sal-B eased H 2 O 2-evoked injury in PC-12 cells. Ascended miR-26a was monitored in Sal-B and H 2 O 2exposed cells. MiR-26a inhibition annulled the protective action of Sal-B in H 2 O 2-corrupted cells. The protective function of Sal-B was enabled through activating PI3K/AKT and MEK/ERK pathways. These findings delineated that Sal-B protected PC-12 cells against H 2 O 2-caused injury through ascending miR-26a via initiating PI3K/AKT and MEK/ERK pathways. HIGHLIGHTS H 2 O 2 causes PC-12 cell injury; Sal-B eases H 2 O 2-caused PC-12 cell injury; Sal-B protects PC-12 cells against H 2 O 2-caused injury via elevating miR-26a; Sal-B activates AKT and MEK/ERK pathways via modulating miR-26a.

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“…in balloon-injured carotid artery rats [29]. MiR-25 is an obbligato miRNA, which has been corroborated to protect PC-12 cells against H 2 O 2 -evoked oxidative damage through Wnt/ b-catenin pathway [30]. Moreover, miR-25 could repress cerebral ischemia/reperfusion injury-evoked cell apoptosis via mediating Fas/FasL pathway [31].…”

Section: Discussionmentioning

confidence: 94%

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

Cao¹,

Fang

Jia

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Emodin (EMO) possesses extensive pharmacological activities, which has been proven to exert the protective impact in diverse nervous system diseases. Nonetheless, whether EMO emerges a neuro-protective activity in hypoxic-evoked ischemic brain injury is still further probed. The intention of the research is to disclose whether EMO emerges neuro-protective activity in hypoxic-evoked ischemic brain injury. PC-12 received hypoxia administration, and then cell viability, apoptosis and autophagy were estimated. After EMO disposition, the above-involved cellular processes were evaluated again. MiR-25 functions in EMO-affected cells were also estimated. The interrelation between miR-25 and neurofilament light-chain polypeptide gene (NEFL) and the conceivable roles of NEFL in hypoxia-disposed cells were investigated. The latent mechanism was uncovered by mTOR and Notch pathways determination. Hypoxia triumphantly triggered apoptosis and autophagy, but EMO repressed these functions in PC-12 cells. Increased miR-25 was induced by EMO, and inhibited miR-25 abated the impacts of EMO on hypoxia-disposed PC-12 cells. NEFL as a neoteric target gene of miR-25 was predicated, and overexpressed NEFL annulled the functions of EMO in hypoxia-injured cells. EMO activated mTOR and Notch pathways through repressing NEFL. The investigations corroborated that EMO weakened hypoxia-triggered injury via elevating miR-25 by targeting NEFL in PC-12 cells.

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MiR-25 protects PC-12 cells from H₂O₂mediated oxidative damage via WNT/β-catenin pathway

Abstract: miR-25 protects PC-12 cells against HO-induced oxidative damage though regulation of Nrf2 and activation of Wnt/β-catenin and PI3 K/AKT/ERK signaling.

Cited by 20 publications

References 40 publications

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

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

Protective functions of salvianolic acid B in PC-12 cells against hydrogen peroxide-triggered damage by mediation of microRNA-26a

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

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MiR-25 protects PC-12 cells from H2O2mediated oxidative damage via WNT/β-catenin pathway

Abstract: miR-25 protects PC-12 cells against HO-induced oxidative damage though regulation of Nrf2 and activation of Wnt/β-catenin and PI3 K/AKT/ERK signaling.

Cited by 20 publications

References 40 publications

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

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

Protective functions of salvianolic acid B in PC-12 cells against hydrogen peroxide-triggered damage by mediation of microRNA-26a

Emodin relieves hypoxia-triggered injury via elevation of microRNA-25 in PC-12 cells

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MiR-25 protects PC-12 cells from H₂O₂mediated oxidative damage via WNT/β-catenin pathway