Protective Effect of Fucoidan against MPP+-Induced SH-SY5Y Cells Apoptosis by Affecting the PI3K/Akt Pathway

Liu, Huaide; Wang, Jing; Zhang, Quanbin; Geng, Lihua; Yue, Yang; Wu, Ning

doi:10.3390/md18060333

Cited by 15 publications

(6 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…inhibitor promoted the activation of the Notch1 signaling pathway, reduced the expression of PTEN and enhanced the activation of Akt, consistent with the study by Zhang et al studies have shown that, following phosphorylation of PI3K and Akt, the target protein Bcl-2 is activated, thereby activating mitochondrial apoptosis. 38,39 These previous findings are consistent with our results. This also partly explains…”

Section: Discussionsupporting

confidence: 93%

miR‐141‐3p regulates saturated fatty acid‐induced cardiomyocyte apoptosis through Notch1/PTEN/AKT pathway via targeting PSEN1

Xin

Duan

Yang

et al. 2021

Environmental Toxicology

View full text Add to dashboard Cite

It has been reported that miR-141-3p levels are markedly upregulated in the cardiomyocytes of obese rats induced by a high-fat diet. However, the role of miR-141-3p in myocardial lipotoxicity remains elusive. In the present study, the role of miR-141-3p in lipotoxic injury of H9c2 cells induced by palmitic acid (PA) and its possible mechanisms were assessed. The results indicated that miR-141-3p was significantly upregulated in PA-induced cardiomyocytes. miR-141-3p inhibitor enhanced the cell viability, reduced the release of lactate dehydrogenase (LDH), creatine kinase-MB (CK-MB), and troponin I (CTN-I), decreased cell apoptosis rate, and repressed the activation of mitochondrial apoptosis pathway in PA-treated H9c2, whereas treatment with miR-141-3p mimics resulted in the opposite effects. Mechanistically, it was further revealed that miR-141-3p could specifically bind to presenilin 1 (PSEN1) 3 0 UTR, and upregulating miR-141-3p levels reduced the expression of PSEN1, thereby inhibiting the activation of the Notch1/PTEN/AKT pathway. Additionally, inhibition of Notch1/AKT signaling pathway by its inhibitor could abrogate the effect of miR-141-3p on mitochondrial-mediated apoptosis induced by PA. In conclusion, the present study demonstrates that miR-141-3p regulates saturated fatty acid-induced cardiomyocyte apoptosis through Notch1/PTEN/AKT pathway via targeting PSEN1, which gains a new insight into the mechanisms of myocardial lipotoxic injury.

show abstract

Section: Discussionsupporting

confidence: 93%

miR‐141‐3p regulates saturated fatty acid‐induced cardiomyocyte apoptosis through Notch1/PTEN/AKT pathway via targeting PSEN1

Xin

Duan

Yang

et al. 2021

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…This study aimed to explore the biological function and specific mechanism of OPA in regulating neuron apoptosis in PD. The present results showed that treating SH-SY5Y cells with MPP + prominently reduced cell viability and induced apoptosis, elevated the level of Bax and Caspase3, but decreased the level of Bcl-2, which were in accordance with the previous reports ( Wang and XU, 2005 ; Kim et al, 2016 ; Kim and Park, 2018 ; Liu et al, 2020b ; Liu et al, 2020c ; Yang et al, 2020 ; Zhou et al, 2021 ). However, according to the experimental results of Hoechst 33342 staining and flow cytometry, the apoptosis of SH-SY5Y cells was remarkably inhibited by the pretreatment of OPA in the PD cell model.…”

Section: Discussionsupporting

confidence: 93%

Neuroprotective Effects of Oligosaccharides From Periplaneta Americana on Parkinson’s Disease Models In Vitro and In Vivo

et al. 2022

View full text Add to dashboard Cite

Parkinson’s disease (PD) is one of the neurodegenerative diseases that is characterized by obvious motor and some nonmotor symptoms. Various therapeutics failed in the effective treatment of PD because of impaired neurological function in the brain and various complications. Periplaneta Americana oligosaccharides (OPA), the main active ingredients extracted from the medicine residues of Periplaneta Americana (P. Americana), have been reported to exert anti-inflammatory effects. The purpose of this study was to evaluate the possible mechanisms of OPA against 1-methyl-4-phenylpyridinium (MPP+)-induced apotosis in SH-SY5Y cells and its potential neuroprotective effects in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced PD subacute model mice. The data demonstrated that OPA significantly reversed the MPP+-induced decrease in SH-SY5Y cell viability, reduced the proportion of apoptotic cells, and protected SH-SY5Y cells from apoptosis in a dose-dependent manner by regulating the expression of apoptosis-related genes. Furthermore, OPA also alleviated the motor dysfunction of PD model mice, prevented the loss of tyrosine hydroxylase positive cells, suppressed the apoptosis of substantia nigra cells, and improved the dysbiosis of gut microbiota in vivo, suggesting that OPA demonstrated a significantly neuroprotective effect on PD model mice. These results indicated that OPA might be the possibility of PD therapeutics with economic utility and high safety.

show abstract

“…Despite increased eEF1A2 levels, PI3K inhibitor-induced cell death was increased. A recent study in MPP + -treated SH-SY5Y cells also found that a PI3K inhibitor LY294002 potentiated apoptosis induced by MPP + , which was accompanied by increased inhibition of phosphorylation of both PI3K and Akt [ 42 ]. Activation of the PI3K/Akt pathway has been shown to inhibit neuronal apoptosis and promote the survival of dopaminergic neurons in a rat model of PD [ 43 ].…”

Section: Discussionmentioning

confidence: 99%

eEF1A2 siRNA Suppresses MPP+-Induced Activation of Akt and mTOR and Potentiates Caspase-3 Activation in a Parkinson’s Disease Model

Khwanraj

Prommahom

Dharmasaroja

2023

The Scientific World Journal

View full text Add to dashboard Cite

The tissue-specific protein eEF1A2 has been linked to the development of neurological disorders. The role of eEF1A2 in the pathogenesis of Parkinson’s disease (PD) has yet to be investigated. The aim of this study was to determine the potential neuroprotective effects of eEF1A2 in an MPP+ model of PD. Differentiated SH-SY5Y cells were transfected with eEF1A2 siRNA, followed by MPP+ exposure. The expression of p-Akt1 and p-mTORC1 was determined using Western blotting. The expression of p53, Bax, Bcl-2, and caspase-3 was evaluated using qRT-PCR. Cleaved caspase-3 levels and Annexin V/propidium iodide flow cytometry were used to determine apoptosis. The effects of PI3K inhibition were examined. The results showed that eEF1A2 siRNA significantly reduced the eEF1A2 expression induced by MPP+. MPP+ treatment activated Akt1 and mTORC1; however, eEF1A2 knockdown suppressed this activation. In eEF1A2-knockdown cells, MPP+ treatment increased the expression of p53 and caspase-3 mRNA levels as well as increased apoptotic cell death when compared to MPP+ treatment alone. In cells exposed to MPP+, upstream inhibition of the Akt/mTOR pathway, by either LY294002 or wortmannin, inhibited the phosphorylation of Akt1 and mTORC1. Both PI3K inhibitors increased eEF1A2 expression in cells, whether or not they were also treated with MPP+. In conclusion, eEF1A2 may function as a neuroprotective factor against MPP+, in part by regulating the Akt/mTOR pathway upstream.

show abstract

Protective Effect of Fucoidan against MPP+-Induced SH-SY5Y Cells Apoptosis by Affecting the PI3K/Akt Pathway

Cited by 15 publications

References 29 publications

miR‐141‐3p regulates saturated fatty acid‐induced cardiomyocyte apoptosis through Notch1/PTEN/AKT pathway via targeting PSEN1

miR‐141‐3p regulates saturated fatty acid‐induced cardiomyocyte apoptosis through Notch1/PTEN/AKT pathway via targeting PSEN1

Neuroprotective Effects of Oligosaccharides From Periplaneta Americana on Parkinson’s Disease Models In Vitro and In Vivo

eEF1A2 siRNA Suppresses MPP+-Induced Activation of Akt and mTOR and Potentiates Caspase-3 Activation in a Parkinson’s Disease Model

Contact Info

Product

Resources

About